Oral Pathology Vimal K Sikri Colour Guides, MCQ's Arpit Sikri

Oral
Pathology
Foreword by
Vimal K. Sikri COLOUR GUIDES

Including MCQ’s
MEDTECH
A Division of Arpit SikriScientific International

Pathology
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Pathology
Foreword by
Dr. Vimal K. Sikri
Director, Punjab Institute of Medical Sciences
Formerly Principal Govt. Dental College and Hospital Amritsar (Punjab)
Dr. Arpit Sikri

Assistant Professor
Sudha Rustagi College of Dental Sciences & Research Faridabad (Haryana)
MEDTECH
Oral
A Division of Scientific International Engaging Sciences—Developing Minds!
Pathology
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Chapter-1 Developmental Defects of Teeth
Aetiology Genetic
Amelogenesis imperfecta—hypoplastic or hypocalcified types

Dentinogenesis imperfecta
Acquired
Rickets
Severe metabolic disturbances
Fluorosis
Tetracycline pigmentation
Microscopy Amelogenesis imperfecta

hypoplastic type—defective matrix formation— enamel irregular, overall thin,
sometimes nodular or pitted but well-calcified, hard and translucent (Fig. 1).
hypocalcified type —normal matrix formation and morphology but soft and
chalky, and readily chipped away.
Dentinogenesis imperfecta: mantle (superficial) dentine
with regular tubules; remainder—a few irregular tubules, inclusion of small

blood vessels (Fig. 2). Enamel defects are also sometimes present.
Rickets: if severe can cause hypocalcification with a wide area of predentine and
many interglobular spaces (Fig. 3).
Severe metabolic disturbances: typically affect enamel matrix producing linear

pitting enamel defects corresponding to degree of tooth formation at time of
illness.
Tetracycline pigmentation: teeth usually of normal form but stained yellow,

degrading to grey or brown. Hard sections show yellow fluorescence along
incremental lines under UV light (Fig. 4).
Fig. 1 Amelogenesis imperfecta: hypoplastic type.
Fig. 3 Rickets.
Fig. 2 Dentinogenesis imperfecta.
Fig. 4 Tetracycline pigmentation.2
Chapter-2 Dental Caries
Aetiology Bacteria: probably mainly acidogenic and glucan- forming strains of

Strep. mutans. Other viridans streptococci, lactobacilli or actinomyces may
contribute, possibly at different stages.
Plaque: adherent meshwork of bacteria in polysaccharides, thickest in

stagnation areas, concentrates bacterial acid production and delays buffering by
saliva (Fig. 5).
Susceptible tooth surface and (possibly) immune responses.

Frequent supply of bacterial substrate—mainly sugar (sucrose).
Enamel caries
Microscopy Pre-cavitation stage: bacterial acid leads to production of increasing

size and numbers of submicroscopic pores in enamel.
Light microscopy shows conical area of change with apex deeply (Fig. 6),
comprising:
dense surface zone (more radiopaque) with enhanced
striae of Retzius
main body of lesion
dark zone
peripheral translucent zone.
Degrees of demineralization in different zones are assessed by polarized light

studies and microradiography. Progressive demineralization eventually allows
entry of bacteria.
Secondary enamel caries: bacteria reach and spread along the amelodentinal
junction (Fig. 7) and attack enamel from beneath over a wide area. The term
secondary enamel caries is also used for caries recurring beside restorations.
Fig. 5 Bacterial plaque on enamel surface.
Fig. 7 Secondary enamel caries.
Fig. 6 Early caries (pre-cavitation stage).
Fig. 8 Caries of dentine.4 Dentine caries
Bacteria spread along the amelodentmal junction (see Fig. 7, p. 4) and down
dentinal tubules. Softening of the matrix by bacterial acids causes distension of
tubules (see Fig. 8, p. 4). Any dentine exposed by enamel destruction is
colonized by plaque, which extends destruction over a wide area (Fig. 9).
Microscopy Dentine is demineralized by bacterial acids from bacteria spreading

along the amelodentinal junction and invades via the tubules, a conical lesion
being formed.
Walls of tubules in softened dentine become distended by bacteria. Intervening

dentine breaks down to form liquefaction foci (Fig 10) and the tissue
progressively disintegrates.
Dentinal reactions
Dead tracts
Odontoblasts are killed in acute caries and pulpal ends of tubules sealed off by
calcified material.
Translucent zones
In very chronic caries or attrition, tubule walls become progressively calcified
(peritubular dentine) until tubules are obliterated (Fig. 11).
Reactionary dentine
Regular tubular dentine forms under chronic lesions. Irregular dentine with few.
irregular tubules forms beneath more acute lesions (Fig. 12).
Fig. 9 Plaque invading dentine.
Fig. 11 Translucent zone.
Fig. 10 Bacteria destroying dentine. (High power.)
Fig. 12 Reactionary dentine.6
Chapter-3
Pulpitis
Aetiology
Microscopy
Caries (most commonly)
Traumatic exposure (cavity preparation, fracture or cracked tooth)

Thermal or chemical irritation, or both, from restorations
Closed pulpitis
Acute closed pulpitis
Typical inflammatory reactions are initially localized to a minute area (Fig. 13)
but typically lead to necrosis of pulp due to restriction of blood supply at the
apical foramen, compression of vessels by oedema in the confined space, and
thrombosis.
All degrees of severity may be encountered, namely: acute hyperaemia and

oedema (Fig. 14)
progressive infiltration by neutrophils
destruction of specialized pulp cells
abscess formation (Fig. 15)
cellulitis (Fig. 16)
necrosis.
(There is little correlation between symptoms and histological picture but acute
pulp pain is usually indicative of irreversibly severe pulpitis.)
Microscopy
Chronic closed pulpitis
Predominantly mononuclear inflammatory cells (lymphocytes, plasma cells and

macrophages).
Initially localized pulp damage. Destruction of pulp is often relatively slow.
Often an incomplete calcific barrier around inflammatory focus.
Usually, necrosis of pulp eventually results.
Fig. 13 Localized pulp abscess.
Fig. 15 Advanced pulp abscess.
Fig. 14 Hyperaemia of pulp.
Fig. 16 Cellulitis of pulp.8 Open pulpitis
Wide exposure of the pulp by carious destruction of the crown may allow it to
survive by relieving the pressure of exudate. Survival of pulp in these
circumstances may be more likely in teeth with open, incomplete apices.
Inflammation extends throughout the pulp, which becomes replaced by
granulation tissue (Fig. 17).
Microscopy Granulation tissue may proliferate through the exposure and become
colonized by epithelial cells. Proliferation of the epithelium may lead to the
formation of an almost complete covering, allowing subsidence of inflammation
beneath (except at the margins in contact with the edges of the carious dentine
and plaque) and progressive fibrosis of the mass. The pulp polyp (Fig. 18) thus
formed appears as a pink or red nodule protruding from a wide exposure.
Destruction of nervous tissue in the mass renders it insensitive.
Other pulp changes

Calcification
Secondary to pulpitis. Calcifications may form at the border of localized low-
grade pulpitis and coalesce to surround it completely (dentine bridge). However,
the bridge is permeable and inflammation extends beneath it (Fig. 19). Dentine
bridges, seen on X-ray after pulp treatment, do not necessarily therefore indicate
complete healing of the underlying pulp.
Diffuse granular calcification. Fine calcifications may progressively extend
through normal pulps and fuse to form large masses (Fig. 20). They are of no
clinical significance.
Pulp stones. Large calcified masses of tubular dentine may form in the pulp,
some at least as excrescences from the walls. They are not necessarily age-
related, and are seen in young persons with the dental abnormalities of Ehlers—
Danlos syndrome. Pulp stones are asymptomatic; their chief significance is
possible obstruction in root canal treatment.
Internal resorption: (see p. 13 and Figs 25-27, p. 14).
Fig. 17 Chronic open pulpitis.
Fig. 19 Calcification (‘dentine bridge’) under pulpitis.
Fig. 18 Open pulpitis; epithelialized polyp.
Fig. 20 Pulp stones and calcifications.10
Chapter-4 Apical Periodontitis
Aetiology Secondary to caries and pulp necrosis in most cases Trauma to tooth
severing apical vessels
Root canal treatment (irritant medicaments or overextension)
Microscopy Acute: accumulation of acute inflammatory cells (neutrophils) and

fluid exudate in potential space between apex and periapical bone (Fig. 21). If
neglected, there is suppuration and resorption, usually of buccal plate of bone,
and sinus formation on the gum overlying the apex of the tooth. In deciduous
molars, inflammation, often interradicular, i.e. overlying permanent successor,
develops.
Chronic: low grade inflammation. Granulation tissue (fibroblasts and capillary

loops) proliferates with varying density of inflammatory infiltrate. A rounded
nodule of granulation tissue (apical granuloma) forms, with resorption of
periapical bone to accommodate it (Figs 22 & 23).
Epithelial content: rests of Malassez are often destroyed by inflammation. If not,

they may proliferate (Fig. 24) in apical granulomas to form microcysts. The
epithelial lining is variable in thickness. Eventually, a radicular cyst may thus
form.
Pus formation: neutrophil infiltration and low grade suppuration usually lead
eventually to discharge via sinus on gingiva or occasionally on skin over apex.
Fig. 21 Acute periapical periodontitis.
Fig. 23 Apical granuloma in situ.
Fig. 22 Apical granuloma.
Fig. 24 Apical granuloma with epithelial proliferation.12 Chapter-5
Resorption and Hypercementosis
Aetiology
Microscopy
Aetiology
Microscopy
Resorption
Normal: in deciduous teeth before shedding
Pathological:
idiopathic—internal or external
secondary (local inflammation, pressure from malposed tooth or tumour,

orthodontic movement, replantation, buried teeth)
Idiopathic: progressive resorption by giant cells, mainly of dentine. There is

sometimes intermittent reparative activity to form a complex pattern of
resorption and bone-like reparative tissue. Resorption (internal or external) can
expose pulp (Figs 25–27). Pulpitis follows.
Secondary: usually localized giant cell activity. Variable reparative activity with
hard tissue deposition is seen.
Hypercementosis
Ageing
Chronic apical periodontitis (adjacent to resorption) Buried teeth, Paget’s
disease
Cementomas (p. 53)
Usually lamellar—sequential deposition of layers of cementum forming smooth

thickening of root. Rarely (Paget’s disease or cementoblastoma), there is an
irregular jigsaw-puzzle (‘mosaic’) pattern of intermittent deposition and
resorption (Fig. 28).
Fig. 25 Internal resorption of dentine.
Fig. 27 Internal resorption showing giant cells.
Fig. 26 External resorption.
Fig. 28 Hypercementosis: lamellar and irregular.14 Chapter-6
Periodontal Disease
Aetiology
Microscopy
Microscopy
15
Normal periodontal tissues

Gingival epithelium comprises:
oral epithelium—extends from mucogingival junction to crest of gingival

margin and has rete ridges
sulcular epithelium—joins the oral and junctional epithelia
junctional epithelium—tends to be flattened and forms a union with the tooth in
the epithelial attachment extending to the amelodentinal junction in normal
mature tissue, apical to which is the periodontal ligament.
Connective tissue gingival fibres support the gingival
margin as a cuff around the tooth. Transeptal fibres
join adjacent teeth and, more deeply, horizontal fibres
join the tooth to the socket wall (Figs 29 & 30 and
Fig. 34, p. 18).
Acute ulcerative gingivitis

Otherwise healthy young adults affected. Aetiology unknown but is associated
with:
poor oral hygiene

smoking
upper respiratory tract infections
stress.
Overwhelming proliferation of Gram-negative anaerobic bacteria traditionally
termed Fusobacterium nucleatum and Borrelia (Treponema) vincentii. Other
anaerobes may also be involved.
A smear shows this fusospirochaetal complex

(Fig. 31) and polymorphs.
Gingival necrosis and non-specific ulceration covered by slough containing

fusiforms and spirochaetes. Tissue is invaded by spirochaetes with progressive
destruction of marginal gingivae (Fig. 32) and then of deeper supporting tissues.
There is no generalized stomatitis.
Fig. 29 Normal human adult buccal gingiva.
Fig. 31 Acute ulcerative gingvitis: fusobacterial complex in samear.
Fig. 30 Normal human adult interdental gingiva.
Fig. 32 Acute ulcerative gingivits: gingival necrosis.16 Chronic gingivitis
Aetiology Inflammatory response to bacterial plaque accumulating at the

gingival margin. The bacterial population is mixed with no specific pathogens
identified although, initially, bacteria are Gram–positive and aerobic. An
increasing bulk of plaque (100–300 cells thick) is associated with increasing
prominence of Gram-negative bacteria, such as veillonellae, fusobacteria and
campylobacter. The process is probably initiated by leakage of bacterial antigens
from plaque in the gingival sulcus.
Microscopy Plaque on tooth surface with inflammation sharply localized to

vicinity of plaque. There is an initial hyperaemic stage (Fig. 33) with relatively
scanty inflammatory cells in the corium. By definition, the periodontal ligament
is not involved and the epithelial attachment to enamel persists despite
inflammatory cells extending beneath it (Fig. 34). The inflammatory infiltrate
becomes increasingly dense but is sharply confined to the marginal gingiva (Fig.
35). It is predominantly lymphoplasmacytic and the protective antibody response
is shown by antibody production in plasma cells (Fig. 36).
Fig. 33 Marginal gingivitis: early hyperaemic stage.
Fig. 35 Marginal gingivitis: dense chronic inflammatory infiltrate.
Fig. 34 Junctional epithelium and epithelial attachment on enamel in gingivitis.
Fig. 36 Immunoperoxidase showing antibody pro18 duction in plasma cells.
Aetiology
Microbiology and immunology
Microscopy
Chronic periodontitis
Persistence of bacterial plaque. Progression of inflammation with tissue

destruction is a common but not invariable sequel to chronic gingivitis; there is
wide individual variation for unknown reasons.
Many potent pathogens (e.g. Porphyromonas species, capnocytophaga,

clostridia, fusobacteria, etc.) can be isolated from periodontal pockets, but
individual roles in tissue destruction are uncertain. Some (e.g. Actinomyces
species) produce bone resorbing factors. A defensive immune response (antibody
production and cellular immunity) to plaque bacteria is detectable. Evidence of
immunologically mediated tissue destruction is speculative only and not
consistent with histological findings. Periodontal destruction is accelerated in
immunodeficient patients but host factors affecting prognosis of periodontal
disease have not been identified in otherwise healthy persons.
1. Plaque and often calculus on tooth surface extending into pockets

(Figs 37 & 38).
2. Predominantly lymphoplasmacytic infiltrate in gingival margin and pocket

walls, not extending more deeply and not involving alveolar bone (Figs 38 &
39).
3. Rootward migration of epithelial attachment (Fig. 40).

4. Destruction of periodontal ligament fibres and alveolar bone, but osteoclasts
rarely seen.
5. Formation of epithelium-lined pockets with epithelial attachment in floor.
Gradual rootward progress of destruction leads eventually to loosening of teeth.
Tissue destruction is usually uniform along the arch (horizontal bone loss) but
local factors may promote more complex patterns of destruction. Localized
destruction of bone around individual teeth (vertical bone loss) may develop or,
occasionally, there is a more rapid destruction of periodontal ligament than
alveolar bone with extension of pocketing between teeth and bone (intrabony
pocketing).
Fig. 37 Chronic periodontitis. Note inflammatory infiltrate localized to vicinity of plaque.
Fig. 39 Chronic periodontits: inflammation-free zone between floor of pocket and bony crest.
Fig. 38 Periodontal pocket: plaque and calculus, and epithelial lining.
Fig. 40 Periodontitis. Migration of epithelial attach20 ment along cementum.
Aetiology
Pathology
Advanced chronic periodontitis
Destruction may progress until tooth support becomes inadequate and more
complex patterns of bone loss develop (Fig. 41).
Intrabony pockets extend deep to the crest of the alveolar bone and are difficult
to manage. Despite the deep extension of inflammation it may remain clear of
the alveolar bone closely adjacent, which may also lack any sign of osteoclastic
activity histologically (Fig. 42).
Periodontal (lateral) abscess
Usually a complication of advanced periodontitis. It may be due to injury to the

pocket floor (food-packing) or more virulent infection.
Rapid acceleration of periodontal destruction. Destruction of epithelial pocket

lining.
Dense neutrophil infiltrate and suppuration (Fig. 43). Widespread osteoclastic
resorption of bone (Fig. 44)
increasing width and depth of pocket to form deep intrabony pocket.

Pus may exude from pocket mouth or point on attached gingiva.
Fig. 41 Late periodontitis with intrabony pocket.
Fig. 43 Periodontal abscess.
Fig. 42 Higher power view of intrabony pocket.
Fig. 44 Giant cells resorbing bony floor of periodon-22 tal abscess.
Aetiology
Microscopy
Microscopy
Gingival recession
Wear and tear from over-vigorous toothbrushing Severe uncontrolled ulcerative
gingivitis
Some cases of chronic periodontitis
Gradual destruction of gingival tissue, periodontal ligament and bone, all at

similar rates. No pocket is formed. There is low grade minimal chronic
inflammation (Fig. 45).
Gingival swelling
Acute myelomonocytic leukaemia
Exaggerated response to plaque, with gross infiltration of gingivae by leukaemic
cells, gingival swelling and accelerated periodontal destruction (Fig. 46).
Fibrous hyperplasia
Hereditary type: generalized smooth gingival swelling may overgrow and
conceal erupting teeth.
Drug-associated hyperplasia: produces bulbous swellings of interdental papillae.

Causes include phenytoin, cyclosporin, nifedipine and its analogues (calcium
channel blockers).
Both show hyperplasia of gingival collagen with ‘stretching’ of elongated rete

ridges
(Fig. 47).
Pregnancy epulis (pregnancy tumour)
Consists of dilated thin-walled vessels in loose oedematous stroma often with
superimposed inflammation (Fig. 48). The condition is not distinguishable from
a pyogenic granuloma except by the pregnant state.
Fig. 45
Gingival and periodontal recession.
Fig. 47 Gingival fibromatosis.
Fig. 46
Acute myelomonocytic leukaemia: gingival infiltration.
Fig. 48
Pregnancy epulis.24
Chapter-7
Cysts of the Jaws
Aetiology
Incidence
Microscopy
25
Radicular cysts (1)
Pulp death, apical periodontitis, proliferation of epithelial rests of Malassez,

cystic change in epithelium; expansion of cyst by hydrostatic pressure;
resorption of surrounding bone.
65–75% of jaw cysts. Radicular cysts are the most common types of cyst and
cause of chronic swellings of the jaws.
Components comprise:
epithelial lining
chronic inflammatory infiltrate
fibrous wall
bony shell undergoing progressive resorption.
The epithelial lining is stratified squamous in type and very variable in

thickness; sometimes with arcaded configuration (Fig. 49), irregularly acanthotic
(Fig. 50) or, rarely, very thick (Fig. 51) In some areas, the epithelial lining may
be destroyed (see Fig. 53, p. 28). The underlying inflammatory infiltrate is also
of variable density. The fibrous wall allows enucleation of the cyst from its bony
shell. Bone shows progressive resorption on the inner aspect and apposition
externally (Fig. 52), but resorption typically outpaces apposition so that the
lateral wall is eventually destroyed.
In the late stages, distension of cyst leads to thinning of the epithelial lining and,
if infection is not superimposed, the inflammatory infiltrate becomes attenuated
(Fig. 52).
Residual cysts
The causative tooth is extracted, leaving a residual cyst. They are typically found
late in life, and show late-type features.
Lateral radicular cysts
These are rare and related to a lateral root canal of a non-vital tooth.
Fig. 49 Arcaded epithelium of cyst lining.
Fig. 51 Radicular cyst. In this example the epithelial lining is conspicuously hyperplastic.
Fig. 50 Inflamed cyst with irregular epithelial lining.
Fig. 52 Complete epithelial, fibrous and bony cyst 26 wall.
Microscopy
Microscopy
Microscopy
Behaviour and prognosis
Radicular cysts (2)
Clefts
Cholesterol from the breakdown of blood cells is frequently seen in cysts as
needle-shaped clefts. Clefts typically form in the cyst wall but extend into the
cyst cavity (Fig. 53, Fig. 58, p. 30). Clefts are surrounded by giant cells whose
cytoplasm becomes stretched and attenuated, but the clusters of nuclei may be
seen near one end (Fig. 54).
Aspiration of cyst fluid typically also shows cholesterol as flat, rhomboid,

notched crystals (Fig. 55) often with many inflammatory cells.
Hyaline bodies
Hyaline (Rushton) bodies are thin refractile rod-like or hair-pin or other shapes
(Fig. 56). Staining is variable. Their nature is unknown. They may be an
epithelial product or haematogenous in origin.
Goblet cells
Mucous metaplasia can produce mucin-filled goblet cells in the epithelial lining
of radicular cysts but considerably more frequently in dentigerous cysts (see Fig.
59, p. 30).
Competent enucleation of radicular cysts is curative. Complications of such

treatment are rare. Neglected cysts can become infected or grow until the jaw
fractures.
Fig. 53 Cleft formation in the wall of a cyst.
Fig. 55 Cholesterol crystal from cyst fluid.
Fig. 54 Clefts in giant cells & deposits of haemosiderin.
Fig. 56 Hyaline bodies in cyst wall.28 Aetiology
Incidence
Microscopy
Microscopy
Dentigerous cysts
Cystic change in remains of enamel organ after completion of enamel formation.

This is a developmental defect of unknown cause.
15–18% of jaw cysts. The male : female ratio is more than 2 : 1.

The cyst wall is attached to the neck of the tooth at or near the amelocemental
junction
(Figs 57 & 58).
The lining of the cyst (probably originating from external enamel epithelium)
typically appears as a thin flat layer of squamous cells without a defined layer of
basal cells. The inner enamel epithelium covering the crown of the tooth is
usually lost. The fibrous wall is typically without inflammatory infiltrate, unless
secondarily infected. Mucous cells are relatively common (Fig. 59).
Competent enucleation of dentigerous cysts with extraction of the contained

tooth is curative. Occasionally, if space is available, the cyst can be
marsupialized and the tooth persuaded to erupt into a functional position.
Eruption cysts
An eruption cyst is, strictly, a soft tissue cyst in the gingiva overlying an
unerupted tooth. It is probably a superficial dentigerous cyst.
Thin fibrous wall with thin squamous epithelial lining deeply and oral mucosal
epithelium superficially (Fig. 60). There is variable inflammatory infiltrate in the
wall.
Eruption cysts usually rupture spontaneously.

Fig. 57 Dentigerous cyst with enamel epithelium between enamel space (left) and cyst (right).
Fig. 59 Goblet cells in dentigerous cyst lining.
Fig. 58 Dentigerous cyst showing attachment at neck of tooth.
Fig. 60 Eruption cyst. Mucosal epithelium covers 30 the roof of the cyst.
Aetiology
Incidence
Radiography
Microscopy
Odontogenic keratocyst
Unknown. Probably originates from primordial odontogenic epithelium (any part

of dental lamina or remnants thereof ) or enamel organ before the start of
amelogenesis. A tooth is sometimes missing.
About 10% of odontogenic cysts. The male to female ratio is about 1.5 : 1. They
form most frequently in young adults or at age 50–60; possibly then as a result
of slow growth and late detection.
About 75% in body or ramus of mandible. Typically, expansive growth into

cancellous bone forms an extensive multilocular area of radiolucency with little
expansion of bone.
Characteristic lining of epithelium of even thickness, 5–8 cells thick, and flat
basement membrane. There is usually a tall, palisaded basal cell layer and thin
eosinophilic layer of parakeratin (Fig. 61).
Orthokeratinization is seen in a minority (about 30%), occasionally with keratin

forming semisolid cyst contents (Fig. 62).
Parakeratinized cysts. The epithelium is typically much folded and tends to

separate from the fibrous wall (Fig. 63). Daughter cysts are occasionally seen in
the cyst wall and may account for some recurrences (see Fig. 65, p. 34). An
inflammatory infiltrate is typically absent but infection and inflammation cause
the lining to resemble that of a radicular cyst (Fig. 64).
Unlike the common odontogenic cysts, keratocysts— particularly the

parakeratinized type—have a strong tendency to recur after treatment,
sometimes decades later. Recurrence rates of up to 60% have been recorded in
the past. The extensive, infiltrative pattern of growth and the weak attachment of
the epithelium to the cyst wall, allowing fragments to be left behind, probably
contribute.
Fig. 61 Typical parakeratinized keratocyst lining.
Fig. 63 Keratocyst, parakeratinized type, showing weak attachment to cyst wall.
Fig. 62 Keratocyst with orthokeratinization.
Fig. 64 Keratocyst showing loss of typical structure 32 as a result of inflammation.
Aetiology
Microscopy
Aetiology
Microscopy
Nasopalatine duct (incisive canal) cyst Proliferation of epithelial remnants of
lining of nasopalatine duct.
Midline cyst of anterior maxilla with lining of squamous and/or ciliated

columnar epithelium (Fig. 66). Characteristically, a neurovascular bundle (also
from incisive canal) (Fig. 67) and sometimes salivary acini may be found in the
cyst wall.
Nasolabial cyst
Unknown. This is an exceedingly rare soft tissue cyst external to the alveolar
ridge beneath the ala nasi. It probably arises from remnants of the lower end of
the nasolacrimal duct. A nasolabial cyst may be seen at almost any age but the
peak incidence is at 40–50 years.
The lining classically (but often not) is of non–ciliated columnar epithelium but
may be squamous or ciliated with a fibrous wall (Fig. 68).
Enucleation is effective.
Fig. 65 Daughter cysts in keratocyst wall.
Fig. 67 Neurovascular bundle in nasopalatine cyst wall.
Fig. 66 Ciliated epithelium lining nasopalatine cyst.
Fig. 68 Nasolabial cyst.34 Microscopy
Incidence
Microscopy
Cystic odontogenic tumours
The main examples are the unicystic ameloblastoma (see p. 44) and the
calcifying odontogenic (ghost cell) cyst.
Cystic ameloblastoma
Extensive cystic change (Fig. 69) can overgrow the tumour. The lining becomes
flattened and may be indistinguishable in part from that of a simple cyst.
Elsewhere, ameloblastoma cells are more obvious in the cyst lining and a typical
tumour forms mural thickening.
Calcifying odontogenic (ghost cell) cyst Rare. Any age can be affected but the
lesion is most often detected in the second decade.
Fibrous wall with lining predominantly of squamous epithelium but the basal
layer cells may be columnar and ameloblast-like. Abnormal keratinization of
spinous cells produces ghost cells consisting of distended eosinophilic epithelial
cells either anuclear or occasionally containing nuclear remnants (Figs 70–72).
Patchy calcification may develop in them. Associated or induced odontogenic
tumours or hamartomas are not infrequent, developing in the adjacent fibrous
wall.
Curettage is usually adequate. Recurrences are uncommon but respond to more

extensive curettage or excision. Spontaneous resolution has occasionally been
reported.
Fig. 69 Cyst in ameloblastoma.
Fig. 71 Calcifying odontogenic cyst with ghost cells.
Fig. 70 Calcifying odontogenic cyst with ghost cells.
Fig. 72
Calcifying odontogenic cyst with ghost cells.36 Incidence and aetiology
Microscopy
Prognosis
Aetiology
Pathology
Prognosis
Cysts without epithelial lining
(non-odontogenic pseudocysts)
Solitary bone cyst
Rare, but with peak age incidence in the second decade. The aetiology is
speculative. Traditionally thought to be traumatic (earlier terms: haemorrhagic or
traumatic bone cyst), but no supporting evidence.
Almost invariably in mandible. The cavity and radiolucency extend through

cancellous bone and arch up between the roots of teeth but rarely expand the
bone.
The cyst may contain serosanguinous fluid or be empty except for air. The wall
is usually rough, bare bone, sometimes with traces of connective tissue as
incomplete lining (Fig. 73), often with evidence of small haemorrhages.
Unlike true cysts, solitary bone cysts probably heal spontaneously. The cavity
should be opened only to confirm the diagnosis. The resulting bleeding into the
cavity causes it to heal, i.e. these cysts are not caused by bleeding into the bone.
Aneurysmal bone cyst
Speculative. Possibly this is a developmental vascular defect or a result of
bleeding into, or vascularization of, a pre-existing lesion such as a giant cell
granuloma.
Grossly, the cyst resembles a blood-filled sponge. Microscopically, it consists of

blood-filled spaces lined by flattened cells and separated by highly vascular
connective tissue septa and similar solid areas often with many giant cells (Figs
74 & 75). Sometimes the solid areas may calcify and resemble ossifying
fibroma.
Excision is usually curative.

Fig. 73 Solitary bone cyst: scanty, incomplete lining (above).
Fig. 74 Aneurysmal bone cyst.
Fig. 75 Aneurysmal bone cyst.38 Chapter-8 Odontogenic Tumours
Ameloblastoma (1)
Most common neoplasm of jaws. Mainly affects males aged over 40 years, with
about 80% of tumours in the ramus or posterior body of the mandible. Typically
appears as a multilocular cyst on a radiograph. Occasionally monolocular, can
mimic a radicular or dentigerous cyst. Slow growing and locally invasive but
does not metastasize.
Microscopy Several subtypes are recognized.
Follicular type: islands or trabeculae of loose angular cells, resembling stellate

reticulum, surrounded by a single layer of tall, columnar, ameloblast-like cells
with nuclei at the opposite pole to the basement membrane (Figs 76–78). Cyst
formation varies from microcysts within a solid tumour to a predominantly
cystic tumour (see Fig. 83, p. 44). Cysts develop either within epithelial islands
(Figs 76 & 77) or from cystic degeneration of connective tissue stroma—only
the ghosts of blood vessels may remain (Fig. 79). In cystic ameloblastoma, the
lining is often flattened, resembling a non-neoplastic cyst (see Fig. 83, p. 44).
Plexiform type: thin trabeculae of epithelial cells in connective tissue stroma

(see Fig. 80, p. 42).
Acanthomatous type: squamous metaplasia of central core of epithelium, but

otherwise resembles the more common follicular type (Fig. 81, p. 42).
Basal cell type: small, darkly staining cells, predominantly in a trabecular pattern
but with little palisading at the periphery. Rare, extraosseous basal cell
ameloblastomas have been mistaken for basal cell carcinomas.
Granular cell type: rare, usually resembles the follicular type, but tumour islands
contain large eosinophilic granular epithelial cells (see Fig. 84, p. 44).
Fig. 76 Ameloblastoma, follicular type.
Fig. 78 Ameloblastoma ameloblast-like cells
Fig. 77 Ameloblastoma, follicular type. Low power view showing follicles of tumour with central
microcyst formation.
Fig. 79 Ameloblastoma showing stromal and epi40 thelial cysts.
Desmoplastic ameloblastomas are rare. Radiographic appearances include

irregular radiolucent areas usually with indistinct borders and containing fine
irregular calcifications. Others are mixed radiolucent/radiopaque with indistinct
borders.
Microscopically, this variant may be difficult to recognize as an ameloblastoma.

Dense collagenous fibrous tissue encloses small, irregular, islands of neoplastic
epithelium. There is little or no cyst formation and ameloblast-like cells are
typically only present in small foci, surrounding some islands of epithelium. The
interior of the epithelial islands consists of densely packed spindle-shaped or
polygonal cells with occasional foci of squamous metaplasia centrally.
Calcification in the fibrous stroma and occasionally bone formation is seen.
Unicystic ameloblastomas are uncommon. They more frequently affect patients

30 years old; males are affected twice as frequently as females.
Unicystic ameloblastoma is defined as a single cystic cavity which shows

ameloblastomatous differentiation in the lining. The unilocular cyst may have a
flattened lining but often with typical ameloblastoma cells in the basal layer only
in some parts, and no infiltration of the wall by neoplasm. Alternatively there
may be intraluminal proliferation without infiltration of the cyst wall. In yet
other cases there may be plexiform or follicular ameloblastoma infiltrating the
cyst wall. In all these circumstances, the lining of the cystic area becomes
flattened and can resemble that of a non-neoplastic cyst. Biopsy of a small part
of the cyst wall therefore may be unrepresentative and lead to it being
misdiagnosed as a non-neoplastic cyst.
The majority surround a misplaced molar tooth and appear radiographically as

dentigerous cysts.
Unicystic ameloblastomas, with no neoplastic infiltration of the cyst wall have a

much better prognosis than conventional ameloblastomas. Even when enucleated
as
41
cysts, the recurrence rate may be only 10%. However, if there is neoplastic
infiltration of the cyst wall, the tumour should be treated as a conventional
ameloblastoma.
Fig. 80 Ameloblastoma, plexiform type.
Fig. 81
Ameloblastoma, acanthomatous type. Squamous epithelium forms the bulk of the central cells.
Fig. 82 Ameloblastoma. Finger-like extensions of tumour appear as islands within the mandibular bone.42
Prognosis
Behaviour
Treatment
Maxillary ameloblastomas are particularly dangerous partly because the bones

are considerably thinner than those of the mandible and offer weak barriers to
spread. Maxillary ameloblastomas tend to form in the posterior segment and to
grow upwards to invade the sinonasal passages, pterygomaxillary fossa, orbit,
cranium and brain, sometimes fatally.
The histological variants of solid ameloblastomas have not been convincingly

shown to affect behaviour and a few have mixed histological patterns. Maxillary
ameloblastomas may be more cellular are more frequently plexiform. They
certainly have a worse prognosis, probably because of the ease with which the
tumour can penetrate the thin maxillary bones to reach the skull base.
Ameloblastomas extending into the soft tissues may also be difficult to manage.
As mentioned earlier, unicystic ameloblastomas frequently respond to
enucleation alone.
Biopsy is essential, particularly for cystic ameloblastomas where a recognizable

tumour may be present only as a limited area of mural thickening.
Differentiation from non-neoplastic cysts or other radiolucent lesions by
radiography alone is unreliable. Ameloblastomas are invasive and recur unless
widely excised. The monolocular, unicystic variant may respond to thorough
enucleation. Rare maxillary ameloblastomas may present major surgical
problems if they invade the cranial cavity. Ameloblastomas spreading into soft
tissues (Fig. 83) are also difficult to manage.
Ideally, treatment is by complete excision, preferably with up to a 2cm margin of

normal bone. However, spread is mainly through cancellous bone and it is
sometimes possible to preserve the lower border of the mandible, if it is tumour-
free, to avoid complete resection of the jaw. Bony repair can re-form much of the
jaw. Any residual tumour is slow growing and any recurrence should be
detectable by regular radiographic follow-up, allowing further limited excision if
necessary.
Fig. 83 Cystic ameloblastoma.
Fig. 84 Ameloblastoma: granular cells.
Fig. 85 Soft tissue extension of ameloblastoma.44 Microscopy
Behaviour
Calcifying odontogenic (ghost cell) ‘cyst’ Solid variant (Fig. 86) of lesion
described earlier (p. 35).
Calcifying epithelial odontogenic

(Pindborg) tumour (CEOT)
This is a rare but important tumour because of its resemblance to and risk of
confusion with poorly differentiated carcinoma. Age and site distribution are
similar to that of ameloblastoma.
Radiographic appearances are variable: there may be circumscribed or diffuse

radiolucency often with scattered snow-shower opacities.
Trabeculation is also variable—multilocular, honeycomb or monolocular

appearances may be seen.
Sheets of variable-sized squamous cells, typically with well-defined cell

membranes and prominent intercellular bridges (Fig. 87). The nuclei are often
pleomorphic, large and hyperchromatic resembling carcinoma (Fig. 88), or
smaller and more uniform (Fig. 89). Variations in appearance do not appear to
affect behaviour. The connective tissue stroma, unlike carcinomas, lacks an
inflammatory infiltrate.
The tumour may also contain calcifications (Fig. 89) and, characteristically,
deposits of amyloid-like material (Fig. 88). A few clear cells may be present but
the clear cell odontogenic carcinoma is a different entity, without amyloid or
calcifications, and can metastasize.
Behaviour of CEOT is rather similar to that of ameloblastoma, with slow but

invasive growth and a tendency to recur if not fully excised.
Fig. 86
Calcifying odontogenic (ghost cell) cyst: solid type showing ameloblast-like cells.
Fig. 88 CEOT. Conspicuous pleomorphism and hyperchromatism of the epithelial nuclei.
Fig. 87 Calcifying epithelial odontogenic tumour. Neoplastic epithelium with large hyperchromatic nuclei
surrounds pinkish amyloid-like material.
Fig. 89 CEOT. Calcifications. 46
Microscopy
Prognosis
Adenomatoid odontogenic tumour
Mainly found in teens or twenties and has a higher incidence in women than in
men. The anterior maxilla is usually affected.
The tumour surrounds, or is contiguous with, a tooth, producing a radiographic

appearance similar to that of a radicular or dentigerous cyst.
Consists of whorls or sheets of small, dark epithelial cells (Fig. 90), frequently
with amorphous or crystalline calcifications and microcysts (resembling ducts in
crosssection) lined by ameloblast-like columnar epithelium (Fig. 91). There is a
fibrous capsule.
The tumour is readily enucleated without risk of recurrence.

Microscopy
Behaviour
Melanotic neuroectodermal tumour of infancy (progonoma)

This is a rare tumour that is not odontogenic but originates from the neural crest.
It is usually detected as a ragged area of radiolucency in the maxilla at about 3
months; the mandible or other sites are rarely affected. Consists of a connective
tissue stroma containing foci of pigmented (melanin-containing) cells (Fig. 92)
with pale nuclei, surrounding small spaces or clefts, together with groups of non-
pigmented cells, alone or surrounded by pigment cells (Fig. 93).
Variable rate of growth, but most appear to be benign and with rare exceptions
do not recur after excision.
Fig. 90
Adenomatoid odontogenic tumour.
Fig. 92 Melanotic neuroectodermal tumour.
Fig. 91 Adenomatoid odontogenic tumour: microcysts and ameloblast like cells.
Fig. 93 Melanotic neuroectodermal tumour: pig48 ment cells. (High power.)
Microscopy
Microscopy
Prognosis
Squamous odontogenic tumour
Rare tumour consisting of multiple islands of welldifferentiated squamous cells

in connective tissue stroma (Figs 94 & 95). It has a wide age distribution and no
apparent sex or site predilection.
This appears to be a tumour of the periodontal ligament epithelium and can

mimic intrabony periodontal pocketing radiographically.
This tumour is benign, and invasion of adjacent structures by maxillary lesions

has rarely been reported. Curettage or conservative resection and extraction of
any teeth involved is usually effective.
Ameloblastic fibroma
Exceedingly rare and typically affects children and teenagers. It forms a slow-
growing, painless swelling with a cyst-like area of radiolucency.
Processes of epithelium resembling ameloblasts surround cells resembling

stellate reticulum (Figs 96 & 97). The stroma resembles dentine papilla (Fig.
97). This is thought to be a true mixed tumour and is sometimes associated with
a developing composite odontoma.
The tumour is readily enucleated but may recur. Sarcomatous change of the
fibrous component is a rare complication.
Fig. 94 Squamous odontogenic tumour.
Fig. 96
Ameloblastic fibroma.
Fig. 95
Squamous odontogenic tumour. (High power.)
Fig. 97 Ameloblastic fibroma. Darkly staining pro-50 cesses of epithelium are surrounded by highly cel
lular mesenchyme.
Microscopy
Treatment and prognosis
Odontogenic myxoma
Probably arises from the mesenchymal component of tooth germ. Usually

detected in the second or third decade, slightly more frequently in the mandible,
as a cystlike or soap bubble area of radiolucency with expansion of bone (Fig.
98).
Loose, mucoid fibrillary tissue contains spindle or stellate cells with long,
delicate, intertwining processes (Fig. 99) and, rarely, rests of odontogenic
epithelium scattered throughout the tumour. Sometimes there is extensive bone
invasion.
Although benign, this tumour is difficult to remove completely and wide

excision is necessary. However, the tumour can persist for years or decades
afterwards, though without necessarily causing symptoms.
Odontomas
These are malformations of developing dental tissues (hamartomas).

Occasionally, an odontoma is associated with a tumour such as ameloblastic
fibroma.
Compound type: multiple small tooth-like structures (denticles) within fibrous

follicles
(Fig. 100).
Complex type: completely irregular mass of dental tissues (Fig. 101). It may
have a cauliflower form with dental tissues surrounding a much branched pulp
chamber. Though lacking any morphological resemblance to a tooth, complex
odontomas have the individual dental tissues in normal relation to one another.
Growth ceases when calcification is complete and the mass tends to erupt and
frequently then becomes infected.
Fig. 98 Odontogenic myxoma.
Fig. 100 Compound odontoma.
Fig. 99 Myxoma: a cellular example.
Fig. 101 Complex odontoma.52 Microscopy
Microscopy
Cementoblastomas and cemental dysplasias
Cementoblastoma
The tumour usually affects males under 25 years. It appears as a radiopaque
apical mass with radiolucent margin, usually in the molar region.
A rounded or irregular mass of cementum can be seen on the root of the tooth
(Figs 102 & 103). The cementum is in a pagetoid (‘mosaic’) pattern with many
cementoblasts (Fig. 104), a peripheral zone of pericementum and a zone of
uncalcified cement matrix (precementum) and fibrous pericementum.
Cementoblastomas are benign but have a potential for continued growth.

However, if the related tooth is extracted and the mass completely enucleated,
recurrence is rare. If incompletely removed, the mass will continue to grow.
Cemento-ossifying fibroma
No useful distinction can be made between cementifying and ossifying fibromas.

Calcifications consist of many cementicle-like ossifications or trabeculae of
bone or, frequently, both. Typically found in the mid-30s ages, women being
twice as frequently affected. The mandible is the usual site.
Radiographically, cemento-ossifying fibromas have well-defined margins and

are radiolucent with varying degrees of calcification. Calcifications tend to be
concentrated centrally. Some specimens appear largely radiopaque with a narrow
radiolucent rim.
A well-defined capsule surrounds connective tissue of variable cellularity,

containing calcifications which also vary widely in type. Calcifications include
trabeculae of woven bone, thicker trabeculae of lamellar bone as well as
dystrophic calcifications. Minute, rounded cementicle- like, acellular
calcifications gradually grow, fuse, and ultimately form a dense mass (Figs 105-
107).
Fig. 102
Cementoblastoma (periphery).
Fig. 104 Cementoblastoma. Cementum-like tissue with may cementoblasts and cementoclasts.
Fig. 103
Cementoblastoma: resorption of related tooth.
Fig. 105
Cemento-ossifying fibroma.54
Microscopy
Prognosis
Cemento-ossifying fibromas can be readily enucleated. Rarely, large

cementoblastomas which have distorted the jaw require local resection and bone
grafting. However if an associated tooth is extracted, a densely calcified
cemento-ossifying fibroma can become a focus for chronic osteomyelitis. If this
happens, wide excision becomes necessary.
Cemento-osseous dysplasias
Cemento-osseous dysplasias comprise florid, focal and periapical types. They

are of periodontal ligament origin. They predominantly affect women, usually
middle-aged, and, overall, blacks are more frequently affected. The mandible is
most frequently involved but florid cementoosseous dysplasia can occupy all
four quadrants.
Cemento-osseous dysplasias are typically asymptomatic and appear

radiographically as moderately welldefined, mottled radiolucent/opaque or more
sclerotic areas of an extent indicated by their names. Periapical cemento-osseous
dysplasia may mimic a periapical granuloma in its early stages. The florid type,
which appears as irregular or lobulated masses without radiolucent borders
interspersed with ill-defined radiolucent/radiopaque areas, may be mistaken for
chronic sclerosing osteomyelitis.
The appearances resemble those of cemento-ossifying fibroma. In the early

stages, cellular fibrous tissue contains foci of cementum-like tissue which grows
and fuses to form a solid, bone-like mass and sometimes, scattered foci of giant
cells (Figs 108-109).
Cemento-osseous dysplasias, once fully calcified, appear to have no potential for

further growth. The main consideration is to distinguish early lesions from
inflammatory disease by dental investigation. Surgical interference, particularly
with florid lesions, should be avoided as it can lead to chronic osteomyelitis.
Fig. 106 Cemento-ossifying fibroma. Fine bone trabeculae surrounded by cellular fibrous tissue.
Fig. 108 Florid cemento-osseous dysplasia. Cellular fibrous tissue containing bony and cementum-like
tissue.
Fig. 107 Cemento-ossifying fibroma. Nodules of cementum-like tissue have fused into large masses.
Fig. 109 Florid cemento-osseous dysplasia. Another 56 area also shows cellular fibrous tissue
containing bony and cementum-like calcifications.
Chapter-9
Nonodontogenic Tumours of Bone
Microscopy
Microscopy
Prognosis
Chondroma
One of the rarest jaw tumours. It consists of hyaline cartilage containing small
chondrocytes in characteristic lacunae. Chondroma is difficult to distinguish
from low grade chondrosarcoma.
Osteochondroma (cartilage-capped osteoma) This is a bony overgrowth with

a cartilaginous cap. 95% of cases arise from the coronoid or condylar process.
Hyaline cartilage, often with regularly aligned cells and resembling an epiphysis,
overlies slowly proliferating bone, usually cancellous in type (Fig. 110). In time,
the mass becomes predominantly bony with a thinning cartilage cap.
Osteoma
May be endosteal or more often periosteal but then it is often difficult to
distinguish from an exostosis. Compact osteoma: lamellae of dense compact
bone with relatively few osteocytes (Fig. 111).
Cancellous osteoma: widely spaced bony trabeculae with cortex of lamellated
bone (Fig. 112).
Osteochondromas and osteomas are benign and excision is effective.
Fig. 100 Osteochondroma.
Fig. 111 Compact osteoma.
Fig. 112 Cancellous osteoma. 58 Radiography
Microscopy
Osteosarcoma
The most common primary tumour of bone. It is a rare complication of

radiotherapy or Paget’s disease of the axial skeleton.
Osteosarcoma usually affects young persons, particularly males.
Radiographic features are highly variable corresponding with the variable

histopathology but there is typically a rapidly growing and painful soft tissue
mass together with a ragged area of radiolucency and variable radiopacity
without definable pattern. Metastasis is mainly to the lungs (Fig. 116) producing
cannon-ball radiopacities.
Appearances are variable and the tumour is either predominantly osteolytic

(undifferentiated) or productive, and then may be predominantly
osteochondroblastic or fibroblastic. It consists of abnormal neoplastic
osteoblasts, which are typically angular, hyperchromatic and larger than normal;
often in large numbers in some areas (Fig. 114). Tumour osteoid (Fig. 113) and
bone are often formed and predominate in the osteoblastic type. Amounts may
be small in the chondro- or fibroblastic variants. Sometimes the tumour is highly
vascular or ‘telangiectatic’. Surrounding normal bone is destroyed (Fig. 115).
Histological characteristics do not seem to correlate well with prognosis.
Osteosarcomas are highly malignant. Wide excision and chemotherapy may

provide a 5-year survival rate of approximately 40% but deaths continue even
after a decade.
Fig. 113 Osteosarcoma with tumour osteoid.
Fig. 115 Osteosarcoma: invasion of normal bone.
Fig. 114 Osteosarcoma: malignant osteoblasts.
Fig. 116 Osteosarcoma: secondary in lung.60 Aetiology
Microscopy
Behaviour
Microscopy
Prognosis
Central giant cell granuloma of the jaws
Unknown; not a neoplasm and not an osteoclastoma. It was mistakenly termed

‘reparative giant cell granuloma’ in the past (but it is more destructive than
reparative). There is no evidence of traumatic aetiology and there are no changes
in blood chemistry. Adolescents or young adults are mainly affected, especially
females, the usual site being the mandible. The tumour produces an area of
radiolucency often with faint trabeculation and indefinite borders or a soap
bubble appearance.
Loose, usually highly cellular and vascular connective tissue stroma containing
multinucleate giant cells of variable size (Figs 117 & 118). The lesions are not
histologically distinguishable from bone lesions of hyperparathyroidism.
Occasionally there is rapid growth and corresponding extension of bone

destruction, but the tumour is benign and responds to conservative resection.
Residual areas may resolve spontaneously.
Multiple myeloma and solitary plasmacytoma
Myeloma is a malignant tumour of plasma cells causing multiple painful

punched-out foci of bone destruction or pathological fractures. Solitary
plasmacytomas are rare and may be in soft tissue. Most ultimately become
multiple.
Occasionally, the condition is detected early, by chance finding of monoclonal

hypergamma-globulinaemia during routine haematological investigation.
The neoplastic plasma cells (Fig. 119) produce monoclonal immunoglobulin—

usually IgG. Amyloid formation (Fig. 120) both within the tumour and in other
sites, such as the tongue, may result.
The median survival for multiple myeloma, even with chemotherapy, is 2–3
years. The 5-year survival rate is less than 20%. Solitary myelomas usually
become multiple within 2–20 years.
Fig. 117 Central giant cell granuloma.
Fig. 119 Myeloma: tumour plasma cells.
Fig. 118 Giant cell granuloma: typical osteoclasts’.
Fig. 120 Myeloma amyloid (green fluorescence with 62 polarized light of Congo Red).
Microscopy
Prognosis
Langerhans cell histiocytosis (histiocytosis X; eosinophilic granuloma)

A rare tumour or tumour-like disease of the Langerhans cells (dendritic, antigen-
presenting cells) causing solitary or multiple areas of destruction of bone and
sometimes of periodontal tissues, exposing the roots of teeth Eosinophilic
granuloma may be solitary or multiple. The mass consists of pleomorphic
‘histiocytes’ and eosinophils in dense clusters or thinly scattered (Fig. 121).
‘Histiocytes’ are typically large and pale and variable in size and shape (Fig.
122) with lobulated nuclei.
Hand-Schüller-Christian disease
Strictly, this is a triad of osteolytic lesions of the skull, exophthalmos and
diabetes insipidus but the name is often applied to any type of multifocal
eosinophilic granuloma. It is a rare variant.
Letterer-Siwe disease
This affects infants or young children. Typically, it also involves soft tissues
(rashes, lymphadenopathy, splenomegaly, fever and anaemia). The prognosis is
poor.
Isolated eosinophilic granuloma typically responds to curettage or may

sometimes resolve spontaneously. In children with widespread disease, the
disease is sometimes fatal despite chemotherapy.
Secondary tumours
Carcinomatous metastases are overall the most common tumours of bone but
considerably less common in the jaws. Secondaries can come particularly from
carcinomas of the breast, lung, prostate, thyroid or kidney and are recognizable
by their resemblance to the primary tumour (Figs 123 & 124). A deposit in the
jaw is very rarely the first sign of a distant asymptomatic primary.
Jaw metastases are typically a sign of disseminated disease and the prognosis is
very poor.
Fig. 121 Eosinophilic granuloma.
Fig. 123 Secondary carcinoma in mandible.
Fig. 122 Eosinophitic granuloma. (High power.)
Fig. 124 Secondary deposit of bronchial carcinoma 64 in jaw.
Chapter-10
Non-neoplastic Bone Diseases
Microscopy
Prognosis
Microscopy
Fibrous dysplasia (monostotic)
Typically seen in young adults of either sex as rounded, painless, smooth bony
swelling of the maxilla. The swelling may disturb function or occlusion.
Radiography shows a rounded area of relative radiolucency often with fine

orange peel or ground glass appearance, but lesions vary from predominantly
fibrous with pseudocystic appearance to patchily sclerotic, and densely ossified.
The borders merge imperceptibly with surrounding normal bone.
Rounded mass of loose, cellular fibrous tissue, typically containing evenly

distributed slender trabeculae of woven bone (Figs 125 & 126) with osteoblasts
within them (Fig. 127), blending imperceptibly with normal bone trabeculae at
margins. The amount of bone is highly variable. Sometimes small foci of
scattered giant cells (Fig. 128) or myxoid tissue can be seen. There are no
significant changes in blood chemistry.
Typically, there is a spontaneous arrest of progress with skeletal maturity.

Resection is only required for disfigurement or disturbed function.
Polyostotic fibrous dysplasia
Onset is often in childhood, predominantly in females. There are multiple lesions

with macular skin pigmentation, endocrine disturbances and precocious puberty
in females in Albright syndrome.
Similar to monostotic type.

Fig. 125 Fibrous dysplasia involving periodontal tissues.
Fig. 127 Fibrous dysplasia: fine trabeculae of woven bone.
Fig. 126 Fibrous dysplasia: trabeculae of woven bone.
Fig. 128 Fibrous dysplasia: small focus of giant 66 cells.
Microscopy
Prognosis
Cherubism (familial fibrous dysplasia) Differs from fibrous dysplasia in:
symmetrical involvement of jaws (mandible, ramus and adjacent body; maxillae

also in severe cases) by giant cell lesions
lesions appear multicystic on radiographs

typically regresses with skeletal maturity
autosomal dominant inheritance but poor penetration of the trait in females and
many sporadic cases. Radiolucencies precede swelling and may persist for
some years after clinical resolution.
Replacement of bone by loose vascular connective tissue containing many giant

cells usually resembling giant cell granuloma (Fig. 129), Histopathology of
cherubism and fibrous dysplasia is not in itself diagnostic.
Confirmation depends on:

clinical picture
radiographic features
behaviour of lesion.
Lesions typically regress completely with skeletal maturation. Treatment of
active disease leads to recurrence.
Aetiology
Microscopy
Prognosis
Hyperparathyroidism
Primary hyperparathyroidism—hypersecretion of parathormone by parathyroid

tumour but bone lesions now exceedingly rare.
Secondary hyperparathyroidism results from renal failure leading to reactive

parathyroid hyperplasia.
Tumour like foci of osteoclasts (Figs 130 & 131) produce
cyst-like areas (sometimes multilocular) on radiographs
(osteitis fibrosa cystica). Microscopically, the condition
is indistinguishable from giant cell granuloma of the
jaws. Diagnosis depends on serum chemistry changes,
namely, raised calcium (up to × 2 normal), normal or low
phosphate and raised alkaline phosphatase.
Removal of the parathyroid tumour leads to resolution of bone lesions.

Fig. 129 Cherubism.
Fig. 130 Hyperparathyroidism.
Fig. 131 Hyperparathyroidism details of osteoclasts.68 Aetiology and prevalence

Microscopy
Prognosis
Paget’s disease of bone (osteitis

deformans)
May be radiologically detectable in 5% of those over 55 in some areas of
Britain, but symptomatic deforming disease is uncommon. The aetiology is
unclear but there is evidence of weak genetic and possibly viral components.
The condition is usually polyostotic and most frequently affects the pelvis,
calvarium and limbs. The maxilla is occasionally affected but the mandible only
rarely. Lesions are predominantly osteolytic initially but there is increasing
sclerosis, often with gross generalized thickening of bone. Alkaline phosphatase
levels are greatly raised (up to × 20 normal).
Radiography. Variable radiolucency of the bone, with loss of trabeculation and

lamina dura, followed by cotton-wool areas of radiopacity and gross, craggy
hypercementosis. In the maxilla, gross thickening of the alveolar ridges causes
the middle third of the face to bulge forward.
Anarchic disorganization of normal bone remodelling results in alternating

resorption and deposition (Fig 132): many osteoblasts and osteoclasts line the
bone margins (Fig. 133). An irregular pattern of reversal lines produces a ligsaw-
puzzle (‘mosaic’) pattern of basophilic lines in the bone, typically with
predominant osteoclastic activity initially, but then with progressively increasing
osteoblastic activity causing bones to become thicker and larger but weaker.
Decreasing vascularity of bones in the late stages makes them susceptible to
infoction. Involvement of cementum produces craggy hypercementosis, which
also shows a ‘mosaic’ pattern microscopically (Fig 134).
The disease is typically active for 3–5 years but may then become virtually static
but leaving persistent deformities.
Sarcomatous change in the axial skeleton is rare and virtually unknown in the
jaws.
Fig. 132 Paget’s disease. Reversal lines form a mosaic’ pattern.
Fig. 133 Paget’s disease of bone: mosaic’ (reversal) lines.
Fig. 134 Paget’s disease: irregular hypercementosis 70 of tooth.
Aetiology
Microscopy
Prognosis
Radiation injury (osteoradionecrosis)
Irradiation for cancer can cause death of bone cells leaving empty lacunae (Fig.
135) and obliterative endarteritis (Fig. 136), leaving severely ischaemic areas of
bone. Attempts to separate this dead tissue by osteoclasts produce moth-eaten
areas but this activity is limited by the poor blood supply. Infection, usually from
teeth, readily spreads in the ischaemic bone and can give rise to extensive
chronic osteomyelitis.
Osteomyelitis
Infection of the jaw can rarely result from severe dental infections or from
fractures open to the skin, or it may be secondary to irradiation.
Infection spreads through the cancellous spaces leading to thrombosis of blood

vessels in bony canaliculae and bone necrosis Necrotic bone shows empty
lacunae, is typically infiltrated by inflammatory cells (Figs 137 & 138) and may
show masses of bacteria. Osteoclasts from healthy peripheral bone resorb the
junction with infected bone which becomes separated as a sequestrum.
After confirming the bacterial cause with a specimen of pus, prompt, vigorous
antibiotic treatment alone is usually effective. Sequestra are typically small and
can be removed when loosened by resorption. Complications include progress to
chronic osteomyelitis or spread of infection causing cellulitis or septicaemia but
are rare.
Osteomyelitis after irradiation is chronic and difficult to eradicate. Hyperbaric

oxygen therapy may be helpful Occasionally it may be necessary to excise most
of the jaw at its healthy margins.
Fig. 135 Osteoradionecrosis.
Fig. 137 Acute osteomyelitis: dead bone and inflammatory cells.
Fig. 136 Irradiation-induced obliterate endarteritis.
Fig. 138 Acute osteomyelitis: acute inflammatory 72 cells in dead bone.
Chapter-11
Infective Stomatitis
Aetiology
Pathology
Aetiology
Microscopy 73
Herpetic stomatitis
A primary infection of a non-immune individual by HSV, usually type 1.

Steadily declining incidence in developed countries but greater prevalence in
immunodeficiency, e.g. AIDS.
Viral infection of epithelial cells produces intra epithelial vesicles (Fig. 139)
with virus-damaged cells in the floor (Fig. 140) leading to epithelial destruction
(Fig. 141), ulcers and inflammation.
Smears from early lesions show ballooning degeneration of epithelial cell nuclei
(Fig. 142
).
There is a systemic febrile illness, lymphadenopathy, and a rising titre of
antibodies.
Oral lesions typically resolve within about a week but malaise may persist
longer. Aciclovir mouth rinses may shorten the illness.
Herpes labialis
Virus may persist in the trigeminal ganglion. Periodic reactivation leads to
vesicles and crusting ulcers on borders of lips in about 30% of patients after
primary infection. Microscopic features are the same as for primary infection.
Herpes labialis typically resolves in about a week but very early application of
aciclovir cream may abort an attack.
Herpes zoster of the trigeminal area
Reactivation of Varicella-zoster infection, usually in the elderly long after the

initial infection (chickenpox). The condition is especially common and severe in
immunodeficiencies; life-threatening in AIDS.
Trigeminal zoster affects the sensory area of skin and mucosa of the affected
division, usually unilaterally and typically with aching pain.
Vesiculation and ulceration, the same as for herpes simplex. Zoster is a disabling
disease in the elderly and requires treatment with aciclovir.
Fig. 139 Herpetic stomatitis: intact vesicle.
Fig. 141 Herpetic stomatitis: necrosis of epithelium.
Fig. 140 Herpetic stomatitis: virus-damaged cells in floor of vesicle.
Fig. 142 Ballooning degeneration of epithelial cells 74 in smear.
Chapter-12
Non-infective Stomatitis
Aetiology
Microscopy
75
Non-specific ulceration can result from trauma or unidentified causes as in
recurrent aphthae.
Recurrent aphthae
Unknown in most cases. Many reported immunological abnormalities, but their

aetiological significance is doubtful. This is not an autoimmune disease—it
affects otherwise healthy persons, and is not associated with recognized
autoimmune diseases. There are no useful immunological diagnostic tests and
there is no reliable response to immunosuppressive treatment.
In 5–10%, ulcers are precipitated by deficiency of, and respond to administration

of, folate, vitamin B12 or occasionally iron.
From 10–20% of the population are affected in some degree. Typically

ulceration starts mildly in childhood or adolescence, often peaks in early adult
life and then gradually declines. Rare onset late in life is usually associated with
a haematinic deficiency state.
Major aphthae, aphthae-like ulcers or ragged necrotizing mucosal ulcers are

sometimes a feature of HIV infection.
Ulceration appears to be preceded by leucocytic infiltration of the epithelium

and underlying corium and intercellular oedema leading to disintegration of the
epithelium (Fig. 143). Ulcers have no specific features but consist of a break in
the epithelium with an intense inflammatory infiltrate extending deeply (Fig.
144). Diagnosis therefore depends largely on the history of regular recurrences
and clinical features.
There is no consistently effective treatment for common aphthae but treatment

with topical corticosteroids, for example, may ameliorate the condition.
Major aphthae, particularly in patients with AIDS, may require treatment with
and respond to thalidomide.
Fig. 143 Aphtha: margin of an active ulcer.

Fig. 144 Aphtha: centre of ulcer.76
Lichen planus
Aetiology Unknown, but some cases are drug induced. Immunological damage
to the epithelium is suggested by the predominantly T lymphocyte infiltrate but
no reason for the lymphocytotoxic reaction has been convincingly demonstrated.
The disease affects otherwise healthy persons and is not associated with typical
autoimmune diseases It is most common after the age of 45, about 65% of cases
are in females. The most frequent clinical manifestation is a lacy pattern of white
striae on the buccal mucosa, typically symmetrically. Other sites include the
margins and dorsum of the tongue or, infrequently, the gingivae (usually atrophic
areas, rarely striae) Atrophic lesions are red and smooth. Erosions typically have
depressed margins and may be covered by a raised layer of yellowish fibrin
White plaques mainly result from longstanding disease Cutaneous lichen planus
is frequently not associated.
Microscopy The inflammatory infiltrate consists mainly of CD4 and CD8 T

lymphocytes However, CD8 T-cells are more numerous in relation to the
epithelium and their numbers rise with disease activity.
Striae (white lesions) . Hyper- or parakeratosis is associated with pointed,

sometimes saw-tooth rete ridges, liquefaction degeneration of the basal cell layer
(see Fig. 148, p. 80) and a band like mononuclear (predominantly T lymphocyte)
infiltrate with a well-defined lower border in the corium (Figs 145 & 146). These
‘classical’ changes rarely seen together.
Atrophic (red) lesions . The epithelium is thin and flattened without keratosis.
The inflammatory infiltrate is more dense but still band like (Fig 147).
Erosions. The epithelium is destroyed by progression of atrophy (not by rupture

of bullae). Secondary infection increases the inflammatory response and
produces a non-specific picture apart from any changes of lichen planus at the
margins.
Fig. 145 Lichen planus.
Fig. 146 Lichen planus: detail of liquefaction degeneration of basal cells.
Fig. 147 Lichen planus: atrophic type. 78

Lichen planus, though usually self-limiting, can persist for many years if
untreated. Frequently, there is a good response to topical corticosteroids:
systemic corticosteroids are usually effective if topical treatment fails.
Approximately 1% risk of malignant change over a 10-year period for specific
sites.
Lichenoid reactions
The term lichenoid reactions sometimes causes considerable confusion, and the
relationship between lichen planus, drug-induced lichen planus and other lichen
planus-like reactions is unclear.
Lichenoid reactions to drugs, amalgams or other restorative materials can

sometimes present ‘classical’ features of lichen planus histologically and there is
considerable overlap between the histological appearances of classical lichen
planus and lichenoid reactions.
Some drug-induced and other lichenoid reactions show greater numbers of

plasma cells superficially in the corium. Perivascular inflammatory infiltrates
and formation of deep lymphoid follicles also suggest a topical or systemic drug
reaction.
Histologically, lichenoid reactions to amalgam can appear the same as those of

idiopathic lichen planus or occasionally similar to those of drug reactions.
Alternatively, there may be prominent lymphoid follicles, neutrophils in the
epithelium and, sometimes, epithelial atypia (Figs 149 & 150).
In view of the difficulty of distinguishing idiopathic from iatrogenic lichen

planus histologically, the diagnosis can be made only with the establishment of a
drug history or of contact of the lesion with a restoration. Confirmation depends
on resolution following withdrawal of the drug or replacement of the restoration.
Fig. 148 Lichen planus, basal cell degeneration (apoptoses).

Fig. 149 Lichenoid reaction.
Fig. 150 Lichenoid reaction to i with deep lymphoid 80 follicles.
Aetiology
Pathology
Microscopy
Prognosis
Bullous erythema multiforme

(Stevens-Johnson syndrome)
Unknown, but occasionally follows drug treatment (especially long-acting
sulphonamides) or herpetic or mycoplasmal infection (primary atypical
pneumonia). However, no triggering factor is identifiable in most cases. No
immunological mechanism has been identified.
The disease typically affects young adults and tends to recur 2 or 3 times a year
and then spontaneously resolves after a time.
This is a mucocutaneous vesiculobullous disease but orolabial lesions alone are

common. Rarely, recently ruptured bullae are seen on the lips but not in the
mouth. Clinically, swollen, bleeding and crusted lips are a typical feature. Oral
ulceration is often widespread but ill-defined and nondescript in character. Target
lesions or bullae affect the skin, and conjunctivitis or iritis may be associated.
Variable picture with degeneration of spinous cells and widespread intercellular

oedema, sometimes leading to intra-epithelial vesiculation or extensive vacuolar
change leading to subepithelial vesiculation (Figs 151 & 152).
Rupture of vesicles leaves erosions. There is a mononuclear inflammatory

infiltrate subepithelially and around superficial blood vessels (Fig. 153).
Orofacial erythema multiforme tends to recur 2–3 times a year but frequently
resolves after a few years. If severe it may respond to systemic corticosteroids or
sometimes to aciclovir. Rarely, it progresses to potentially fatal multisystem
disease with malaise and fever and toxic epidermal necrolysis or fatal renal
disease.
Fig. 151 Bullous erythema multiforme, early stage.
Fig. 152 Erythema multiforme: higher power.
Fig. 153 Erythema multiforme: perivascular inflammatory infiltrate.82 Aetiology and

pathology
Microscopy
Prognosis
Pemphigus vulgaris
A ‘typical’ autoimmune disease with circulating autoantibodies against the

epithelial intercellular adhesion molecule, desmoglein 3, which can be
demonstrated in situ by immunofluorescence. Destruction of intercellular
adherence leads to disintegration of epithelia and intra-epithelial vesiculation,
often first in the mouth.
Clinically, women are more frequently affected, usually between the ages of 40
and 50, sometimes with oral lesions as the first sign. Vesicles are fragile, rarely
seen intact in the mouth, but they typically leave small, painful irregular
erosions. Occasionally, vesicles are produced by stroking the mucosa
(Nikolsky’s sign). Bullae are obvious on skin and can spread over the whole
body. Rupture leaves crusted lesions.
Separation of epithelial cells from one another (acantholysis) initially forming

suprabasal clefts then intraepithelial vesicles. Basal cells adhere to one another
and to underlying connective tissue to form the floor of vesicles but they
eventually separate after rupture of vesicles (Fig. 154) to leave ulcers with
inflammatory infiltrate in the floor. Prickle cells after acantholysis become
rounded, float off in vesicle fluid (Fig. 155) and are seen in smears (Tzanck
cells).
There is positive immunofluorescence of immunoglobulin (usually IgG) along

intercellular junctions and coating detached acantholytic cells.
Absolute confirmation of the diagnosis is possible by immunofluorescence for

immunoglobulin (Fig. 156), but histology is frequently adequate.
Cutaneous fluid and electrolyte loss or infection are usually fatal if untreated.
Immunosuppressive treatment is life-saving but heavy doses of corticosteroids
and azathioprine are required. Relapse frequently follows withdrawal of
treatment but deaths are mainly a complication of immunosuppression and
frequently result from infection. The overall mortality long term is about 6%.
Fig. 154 Pemphigus vulgaris: recently ruptured vesicle.
Fig. 155 Pemphigus vulgaris: acantholytic cells separating from each other—early stage.
Fig. 156 Pemphigus vulgaris: immunofluorescence 84 showing binding of antibody to intercellular
adhesion
molecules.
Aetiology and pathology
Microscopy
Prognosis
Mucous membrane pemphigoid
There is some evidence for immunopathogenesis with formation of antibodies

against the basement membrane zone (BMZ). Women are mainly affected
between the ages of 50–70 years.
Bullae and vesicles result from loss of attachment of epithelium to the

underlying connective tissue. Bullae result from minor trauma; Nikolsky’s sign
may be positive; ruptured vesicles leave indolent erosions; lesions on gingivae
may be called desquamative gingivitis’. Scarring (and damage to sight) is
common in the ocular variant but rare in the mouth.
Subepiderma! bulla separating full thickness of epithelium from lamina propria.

No acantholysis.
Mixed, chronic inflammatory infiltrate in lamina propria (Figs 157 & 158).
Electron microscopy shows the level of separation
of the epithelium to be along the lamina lucida (between the plasma membrane
of the basal cells and the
electron-dense basal lamina).
Autoantibodies to basement membrane zone material (anti-BMZ ab) are not

routinely detectable in serum: immunofluorescence to immunoglobulins along
the BMZ is seen in about 40% but the complement component (C3) is seen in
about 80% (see Fig. 159, p. 88). There is a poor correlation between anti-BMZ
ab titres and the severity of the disease as assessed by routine methods. There is
no recognized association with other more typical autoimmune diseases.
The disease is persistent but benign and oral lesions frequently respond to topical
corticosteroids. Systemic steroids may sometimes be required particularly for
ocular involvement.
Fig. 157 Mucous membrane pemphigoid. Separation of full thickness of the epithelium from the corium.
Fig. 158 158 Mucous membrane pemphigoid (High 86 power.)
Localized oral purpura (‘angina bullosa haemorrhagica’)

Purpura localized to the oral cavity (i.e. in the absence of a haemostatic defect)
causes blood blisters, probably because of some local defect of blood vessels.
Rupture of the roof of the blister leaves a painful ulcer. In the throat this can
cause a choking sensation (‘angina’) (Fig. 160).
Localized oral purpura must be distinguished from the blisters of pemphigoid

which sometimes fill with blood.
Fig. 159 Mucous membrane pemphigoid: immunofluorescence of complement (C3) along basement
membrane zone.
Fig. 160 Localized oral purpura. Blood blister due to subepithelial leakage of blood.

Microscopy
Treatment
Lupus erythematosus
Either systemic or discoid lupus erythematosus (SLE or DLE) can cause oral
lesions.
SLE is a connective tissue disease (autoimmune), thought to be immune-

complex mediated, with multiple non-organ-specific autoantibodies, particularly
antinuclear factors and often rheumatoid factor. Common effects are rashes and
arthritis but almost any system can be involved and Sjögren syndrome is present
in about 30% of cases.
DLE is mucocutaneous with lesions appearing the same as those of SLE, but
minimal systemic effects or autoantibody production.
Women aged 20–40 years are mainly affected. Oral lesions consist of streaky
white or erythematous areas, or erosions frequently similar to those of lichen
planus.
Highly variable picture with highly irregular patterns of acanthosis or epithelial

atrophy, liquefaction degeneration of the basal cell layer and widely scattered
inflammatory infiltrate in the corium (Figs 161 & 162). Thickening of the
basement membrane zone is shown by PAS staining (Fig. 163). Immunoglobulin
and complement are also detectable there by immunofluorescence.
Diagnosis of SLE should be confirmed by autoantibody studies, which

differentiate it from DLE.
Lesions often respond poorly to topical corticosteroids, but systemic

corticosteroids are justifiable for extensive SLE.
Fig. 161 Lupus erythematosus.
Fig. 162 Lupus erythematosus.
Fig. 163 Lupus erythematosus: basement membrane deposits of antigen/antibody (PAS stain.)90
Chapter-13
Keratoses (leukoplakias; white lesions)
Terminology
Microscopy
Leukoplakias are chronic white (keratotic) mucosal plaques which are not due to
any identifiable disease. The term is purely clinical and has no histological
implications, but histology is necessary to exclude malignancy or other diseases.
Most leukoplakias are not premalignant but red lesions (erythroplasias; p. 107)
are frequently severely dysplastic or invasive carcinoma.
Oral white plaques share many histological features, and idiopathic forms are
often not distinguishable histologically from those with defined causes such as
frictional keratosis, but may show dysplasia microscopically. Features of oral
white lesions include the following in varying combinations:
Hyper(ortho)keratosis: a superficial eosinophilic layer
of dead epithelial squames under which there is a layer of epithelial cells
containing basophilic granules of prekeratin (Fig. 164).
Parakeratosis: the surface consists of effete epithelial cells containing shrunken,

pyknotic, basophilic nuclei with no underlying granular cell layer (Figs 165 &
166).
Acanthosis: hyperplasia of the prickle cell layer usually with loss of the
normally regular profile of the rete ridges (Fig 165).
Epithelial atrophy: thinning usually with loss of the rete ridges of the epithelium
(Fig. 167).
Dysplasia (see pp. 105-106) may be associated with keratosis but there is no
consistent relationship.
Fig. 164 Hyper(ortho)keratosis.
Fig. 166 Parakeratosis detail.
Fig. 165 Parakeratosis and acanthosis.
Fig. 167 Hyperorthokeratosis and epithelial atrophy.92 Aetiology and pathology
Microscopy
Prognosis
White sponge naevus
Hereditary (autosomal dominant) disorder producing soft, white thickening of

the oral mucosa. The condition is asymptomatic (may not be noticed until
adulthood), but tags of protruding epithelium may be chewed off or detached,
producing an irregular surface. The whole of the oral mucosa may be affected to
variable degree.
Typically regular acanthosis with widespread intracellular oedema extending

particularly in the plaque where prominent cell membranes give a ‘basket-
weave’ appearance (Figs 168 & 169). The surface is typically irregular.
Inflammatory infiltrate is absent from the corium (Fig. 170).
The condition is benign and once the diagnosis is confirmed by histology, only
reassurance is required.
Fig. 168 White sponge naevus.
Fig. 169 White sponge naevus: oedematous epithelial cells.
Fig. 170 White sponge naevus: partial detachment of plaque.94 Microscopy
Leukoedema
Leukoedema is an anatomical variation consisting of a translucent, filmy

thickening of the mucosa, most common in blacks.
Frequently, mild acanthosis with vacuolation of the superficial prickle cells (Fig.
171) gives a mild basket weave appearance, but less extensive than that seen in
white sponge naevus (see Fig. 168, p. 94).
Leukoedema is of no clinical significance.

Microscopy
Cheek-biting
Cheek biting is a moderately common habit which may be a response to anxiety

or used during periods of mental concentration. Clinically the buccal mucosa
appears rough, with red areas and small tags of white thickened mucosa.
There is acanthosis and a thick, ragged parakeratinized layer on which there may
be conspicuous bacterial colonization (Fig. 172). Occasionally the epithelium
may contain koilocyte- like cells (Fig. 172) and bear some resemblance to hairy
leukoplakia. However, the clinical features are significantly different.
Clinically, cheek-biting is of little clinical significance, though it may be

confused with other white patches. The patient may require reassurance and be
advised to be aware of the needlessness of the habit.
Fig. 171 Leukoedema Vacuolation of the prickle cells.
Fig. 172 Cheek-biting. Colonies of bacteria have infected the parakeratotic epithelium.
Microscopy
Erythema migrans
Erythema migrans (geographical tongue) appears to be an anatomical variant,

though in about 5% there is an association with psoriasis. Also, there appears to
be a genetic component and the abnormality may be seen in more than one
member of the family or in several generations.
Clinically, children, and even very young infants, can be affected, but it seems
rarely to be noticed then and most patients are middle aged. Fissuring of the
tongue may be associated, and adults particularly may complain of soreness. The
tongue, and rarely other mucosal sites, show irregular red areas sometimes with
a conspicuous slightly raised white margin forming scalloped patterns. The
characteristic feature is the change in these appearances from day to day as the
areas spread or recede over the mucosa.
The appearances vary. Commonly, the central red areas are atrophic while the
advancing margins show acanthosis, with oedema and neutrophil infiltration of
the epithelium, giving an appearance similar to candidosis but without fungal
hyphae. There is a variable inflammatory infiltrate in the corium (Fig. 173).
Treatment is not required but reassurance may need to be given.

Fig. 173 Erythema migrans. Acanthotic, advancing margin.
Prognosis
Frictional keratosis
This shows non-specific keratosis microscopically (Fig. 174) and is

distinguishable only by clinical evidence of mechanical trauma and resolution
with removal of the irritant.
Resolution quickly follows removal of the irritant and confirms the diagnosis.
Microscopy
Prognosis
Microscopy
Prognosis
Smoker’s keratosis
This results from heavy long-term pipe smoking, is therefore seen in men, and
affects the palate.
The keratosis is non-specific but there is characteristically inflammation and

swelling of the palatal mucous glands producing red umbilicated swellings (Fig.
175).
Prolonged pipe smoking is associated with a raised risk of cancer. However, the
palatal white lesion is benign and any oral carcinoma that develops usually
appears lower in the mouth such as the retromolar region.
Syphilitic leukoplakia
A feature of the tertiary stage of syphilis but rarely seen now. It typically affects
the dorsum of the tongue and there is a high risk of malignant change.
Features of epithelial keratosis are not specific but dysplasia or malignant

change may be evident
(Fig. 176).
A characteristic syphilitic inflammatory response (endarteritis (Fig. 177), plasma

cell infiltrate and occasionally granuloma formation) may be seen deeply, but
diagnosis is essentially serological.
The risk of malignant change in syphilitic leukoplakia is very high.

Fig. 174 Frictional keratosis.
Fig. 176 Syphilitic leukoplakia with mild dysplasia.
Fig. 175 Smoker’s keratosis: swollen palatal salivary tissue.
Fig. 177 Endarteritis beneath syphilitic leukoplakia.100
Aetiology
Microscopy
Treatment
Acute candidosis (thrush; ‘pseudomembranous’ candidosis)

Thrush is the typical acute infection of mucous membranes by Candida albicans.
It implies underlying immunodeficiency, e.g. neonates, HIV infection, prolonged
broad spectrum antimicrobial, immunosuppressive and cytotoxic treatment or
debilitating illness.
Clinically, thrush forms soft friable, creamy flecks or plaques that wipe off easily
revealing intact but erythematous epithelium A Gram-stained smear shows many
Gram-positive hyphae of C. albicans and inflammatory cells (Fig. 178).
The plaque of thrush is due to epithelial proliferation, i.e. it is not a

pseudomembrane (adherent slough). The epithelial cells of the plaque are
separated by inflammatory exudate (hence it is friable) including many
neutrophils.
The inflammatory infiltrate is most dense, forming microabscesses, at the

surface of the prickle cell layer and provides the plane of cleavage that allows
the plaque to be wiped off. PAS staining demonstrates candidal hyphae growing
downwards through the epithelial cells to the surface of the spinous cell layer
(Fig. 180). Deeply, there is acanthosis with long, slender downgrowths of
epithelium, and inflammatory cells infiltrating the lamina propria (Fig. 179).
Thrush frequently responds well to topical antifungals such as nystatin or

amphotericin but in severe immunodeficiency (e.g. HIV infection) fluconazole
may be needed.
Fig. 178 Thrush: tangled hyphae in smear (Gram stain.
Fig. 179 Thrush: plaque. (PAS.)
Fig. 180 Thrush: hyphae in plaque. (High power; PAS.)102
Microscopy
Microscopy
Chronic hyperplastic candidosis (candidal leukoplakia)

Uncommon, persistent candidal infection usually of middle age or over but
occasionally seen in patients with HIV infection, who may develop any type of
oral candidosis. Clinically, chronic candidal plaques may be homogeneous or
speckled.
Production of parakeratotic plaque. Hyphae grow through plaque to the spinous
layer (Figs 181 & 182). Plaque is infiltrated by moderate numbers of leukocytes
and beads of oedema. The deeper epithelium is acanthotic, sometimes grossly so
(Fig. 183), and sometimes dysplastic.
Chronic mucocutaneous candidosis syndromes

All are rare but comprise leukoplakia-like oral candidosis associated with
variable skin and nail involvement, and sometimes systemic disorders. There is a
limited defect of cellular immunity in about 60% of patients but no special
susceptibility to systemic candidosis One variant is associated with endocrine
deficiencies, particularly primary hypoparathyroidism and Addison’s disease
(candida endocrinopathy syndrome).
As for isolated chronic candidosis (see Figs 181–183).

Microscopy
Denture-induced erythematous candidosis
Most common under an upper denture where hyphae of C. albicans proliferate in

the interface between denture base and mucosa, which is cut off from local
defenses. Diffuse candidal erythema is also seen in xerostomia.
In HIV infection C. albicans can cause red mucosal macules (erythematous

candidosis).
Hyphae are superficial to the epithelium and not seen in sections. The epithelium
is spongiotic, acanthotic and infiltrated by chronic inflammatory cells.
103
Hairy leukoplakia See pages 159–160.
Fig. 181 Chronic candidosis: hyphae invading parakeratotic plaque. (PAS).
Fig. 182 Chronic candidosis: hyphae and inflammatory infiltrate in plaque.
Fig. 183 Chronic candidosis: plaque and gross acanthosis.104 Microscopy
Dysplasia (epithelial atypia; dyskeratosis)
Dysplasia is abnormal maturation and differentiation of the epithelium, as seen

in carcinomas and also in some leukoplakias, when it is usually an indication of
premalignancy.
The following features are seen in varying combinations. Hyperchromatism and

alteration of the nuclear cyto
plasmic ratio. Nuclei are abnormally large in relation
to the area of cytoplasm and more heavily basophilic.
Nucleoli may be more prominent or numerous. Nuclear pleomorphism
(irregularly shaped nuclei) is often
associated (Fig. 184).
Individual, deep cell keratinization (dyskeratosis). Individual cells within the
prickle cell layer develop intracytoplasmic keratin and become eosinophilic (Fig.
185).
Loss of polarity. The basal cell layer loses its normal
orderly arrangement and the cells lie irregularly at
angles to one another (Figs 185 & 186).
Mitoses. These may be seen superficially among the
spinous cells and are of sinister import, particularly if
abnormal.
Other features. Loss of intercellular adherence with
fluid-filled spaces appearing between the epithelial
cells (Fig. 186) and drop-shaped (bulbous) rete ridges
are sometimes associated with dysplasia. Hyperkeratosis and/or acanthosis may
or may not be associated.
Severe dysplasia with cellular abnormalities extending through the full thickness
of the epithelium (top-tobottom change) is sometimes termed carcinoma-in-situ
(Fig. 187), i.e. the cellular abnormalities of carcinoma are present but there is no
invasion.
Dysplasia indicates a strong risk of malignant change. However, some dysplastic
lesions undergo spontaneous regression and the level of risk is unpredictable
even from the histological findings. The assessment of the latter is also highly
subjective.
Fig. 184 Mild to moderate dysplasia with hyperchromatism and hyperkeratosis.
Fig. 186 Dysplasia: loss of intercellular adherence.
Fig. 185 Dysplasia with deep cell keratinization: hyperchromatism and loss of polarity.
Fig. 187 Severe dysplasia (top-to-bottom change, 106 carcinoma-in-situ).
Microscopy
Microscopy
Treatment
Erythroplasia (‘erythroplakia’)
This is a clinical term for chronic red lesions (i.e. hyperkeratosis is absent). They
do not form raised plaques but are typically level with, or depressed below, the
surrounding mucosa and typically show severe dysplasia (Fig 188) or early
carcinoma.
Early keratinizing carcinoma
In addition to dysplastic leukoplakias, some early carcinomas, before ulcerating,

produce keratin on the surface and appear clinically as innocent white lesions.
Invasive squamous cell carcinoma replaces the normal epithelial surface with an
overlying parakeratinized plaque (Fig. 189).
Squamous cell papilloma
A common, benign lesion characterized by fine, fingerlike papillae, giving it a

warty appearance clinically. HPV (particularly types 6 and 11) may be
implicated, but cytological signs of viral infection are not seen histologically.
Oral viral warts resemble papillomas clinically, but show viral changes and
inclusion bodies histologically.
A central branching core of vascular connective tissue extends into the papillae.
The latter are covered by hyperplastic stratified squamous epithelium which may
be keratinized (Fig. 190).
The papilloma then appears white.

Excision is curative.
Fig. 188 Erythroplasia.
Fig. 189 Carcinoma with keratinized surface.
Fig. 190 Squamous cell papilloma.108
Chapter-14
Squamous Cell Carcinoma
Microscopy
Aetiological factors usually unidentifiable although widely regarded as related to

tobacco and alcohol use. There is a closer relationship with pipe than cigarette
smoking. The high incidence of oral cancer in India is possibly related to
different types and forms of tobacco usage. HPV 16 and related strains have
been implicated, possibly by triggering inactivation of the p53 gene. Squamous
cell carcinoma usually develops after age 50 and the incidence rises with age.
Lip cancer is associated with excess exposure to sunshine, especially in fair

skinned males. It is associated with leukoplakia in only a minority.
Essential features are epithelial abnormalities (dysplasia) and invasion. Later,

metastases develop, particularly in regional lymph nodes. Most are well
differentiated with obvious squamous pattern and formation of whorls of keratin
deeply (cell nests) (Fig. 191).
The basement membrane tends to disappear and the tumour forms invading,
irregular epithelial processes or sheets of cells with ill-defined outlines typically
surrounded by chronic inflammatory cells (Fig. 192). Invasion is characterized
by destruction of tissues in the path of the tumour (Fig. 193).
Neoplastic epithelial cells are pleomorphic, show variably enlarged, often

hyperchromatic, nuclei or vesicular nuclei with prominent or multiple nucleoli
(Fig. 194). Mitoses (see Fig. 195, p 112) may be numerous and atypical. With
increasing dedifferentiation, the neoplastic cells may become progressively more
uniformly hyperchromatic and irregular in size so that they may become difficult
to recognize as carcinomas by light microscopy in extreme (anaplastic)
examples. Spread is primarily via lymphatics, but haematogenous spread to
distal sites depends on invasion of blood vessels (see Fig. 196, p. 112).
Fig. 191 Oral squamous cell carcinoma.
Fig. 193 Squamous carcinoma destroying muscle
Fig. 192 Squamous cell carcinoma: well-differentiated.
Fig. 194 Squamous carcinoma, atypia.110
Microscopy
The main forms of treatment are wide excision often with radiotherapy, or
radiotherapy alone. Good survival rates depend on early diagnosis and treatment.
Survival also deteriorates with age. Average 5-year survival rates for carcinoma
of the tongue are 37% for males and 46% for females. Most other sites within
the mouth have a rather better prognosis.
Carcinoma of the lip has a much better prognosis and a 5-year survival rate of
94% for males but (inexplicably) only 84% for females.
Verrucous carcinoma
An uncommon variant which appears as a prominent white warty plaque. It may

result from the prolonged use of smokeless tobacco (snuff dipping) but
frequently no cause is apparent. HPV 2a-e may be implicated.
Gross hyperkeratosis and papillary epithelial overgrowth produces a folded

appearance with intervening cleft-like spaces. The uniform level of downgrowth
of the tumour gives a well-defined deep margin in the pre-invasive stage (Fig.
197), but can transform to invasive carcinoma. Epithelial atypia is minimal (in
the early stages), but there is typically a chronic inflammatory infiltrate in the
corium.
Spread and metastasis is slower than squamous cell carcinoma and the response
to adequate excision is better.
Verrucous hyperplasia
An essentially similar lesion to verrucous carcinoma but differing histologically

in that the mass does not push down into the lamina propria and the basement
membrane zone is level with that of the surrounding normal epithelium.
Fig. 195 Squamous carcinoma: abnormal mitoses.
Fig. 196 Squamous cell carcinoma: tumour extending along a vein.
Fig. 197 Verrucous carcinoma.112 Chapter-15
Hyperplastic Lesions
Microscopy
Treatment
Fibrous nodules (fibrous epulides, polyps and denture granulomas)
These are some of the most common oral swellings but are hyperplastic, not
neoplastic, resulting from fibrous proliferation in response to chronic irritation
often with an inflammatory component.
These lesions are distinguishable only by their site of origin and consist of
irregular bundles of collagenous connective tissue with varying numbers of
fibroblasts covered by stratified squamous epithelium (Figs 198–200), often with
mild subepithelial inflammatory infiltrate. Osteoid or bone may form within a
fibrous epulis (Fig. 201). More severe and deeply extending inflammation results
from ulceration.
Adequate excision should be curative.
Microscopy
Treatment
Pyogenic granuloma
Clinically, pyogenic granulomas appear as soft, red nodules, usually on the

gingival margins. Despite their name, these are vascular proliferations, but
inflammation is frequently superimposed.
Many dilated thin-walled blood vessels lie in a loose connective tissue stroma
but typically, inflammatory cells fill the vessels and infiltrate the stroma (see Fig.
202, p. 116). The nodule is covered by stratified squamous epithelium of
variable thickness and, particularly in the inflamed type, may be ulcerated.
Excision is curative.
Fig. 198 Fibrous epulis.
Fig. 200 Fibrous nodule: general structure.
Fig. 199 Fibrous polyp of cheek.
Fig. 201 Fibrous epulis with ossification.114 Treatment and prognosis
Pregnancy epulis
During pregnancy, hormonal factors favour gingival hyperplasia and formation

of pyogenic granulomas (pregnancy epulis). Clinically and histologically these
do not differ from pyogenic granulomas seen in non-pregnant persons—only the
pregnant state differentiates them (Fig. 203).
Pregnancy epulis is likely to regress after parturition if oral hygiene is good, but
may have to be excised.
Microscopy
Treatment
Giant cell epulis
This hyperplastic lesion is believed to result from a proliferation of osteoclasts

from the sites of shedding of deciduous teeth as it is only found in this area of
the alveolar ridge and mainly in young people. Exceptionally rarely,
hyperparathyroidism gives rise to a giant cell epulis, distinguishable only by
abnormal blood chemistry and bone lesions, if present.
The highly cellular mass is crowded with osteoclast-like giant cells of variable
size in a cellular and vascular stroma and covered by stratified squamous
epithelium (Figs 204 & 205).
If neglected, it may undergo gradual fibrosis with a shrinking core of giant cells
surrounded by fibrous tissue. Excision is curative.
Fig. 202 Pyogenic granuloma.
Fig. 204 Giant cell epulis.
Fig. 203 Pregnancy epulis.
Fig. 205 Giant cell epulis. (High power.)116 Chapter-16
Benign Connective Tissue Tumours
Microscopy
Microscopy
Neurofibroma
Neurofibromas are uncommon tumours arising from nerve sheath fibroblasts.
They consist of wavy bundles of collagen and fibroblasts with elongated nuclei
(Fig. 206). Variable amounts of mucinous ground substance are present and may
produce a myxoid appearance. The tumour may contain nerve fibres or be
continuous with the sheath of a nerve.
Oral neurofibromas are rare and frequently associated with neurofibromatosis.

Neurilemmoma
Neurilemmomas arise from Schwann cells which form the axonal sheath.
They characteristically comprise two types of tissue:
Antoni A tissue—consists of regularly arranged elongated spindle cells with

closely aligned (palisaded) nuclei which are darkly basophilic and elongated
(Fig. 207).
Antoni B areas—consist of shorter spindle-shaped or oval cells in a mucinous

matrix and wavy delicate bundles of collagen fibres.
Traumatic (amputation) neuroma
Proliferation of fibres from the proximal stump of a severed nerve can produce a
tumour-like nodule of nerve fascicles surrounded by fibrous tissue (Fig 208).
Isolated neurofibromas, neurolemmonas and traumatic neuromas are benign and

respond to excision.
Fig. 206 Neurofibroma.
Fig. 207 Neurilemmoma.
Fig. 208 Traumatic neuroma.118 Microscopy
Plexiform neurofibroma
This consists of a tangled mass of nerve fibres cut in various planes (Fig. 209). It
can be solitary but is a characteristic feature of neurofibromatosis type 1 (von
Recklinghausen’s disease). When found in the lateral border of the tongue,
particularly, this lesion is likely to be one of the features of multiple endocrine
neoplasia and associated with phaeochromocytoma and medullary carcinoma of
the thyroid.
Haemangiomas
These are usually hamartomas rather than true tumours and are sometimes part
of a widespread developmental defect (mucocutaneous angiomatosis, portwine
stain).
Capillary haemangiomas
These consist of a mass of fine capillaries or imperforate rosettes of endothelial
cells (Fig. 210), covered by squamous epithelium.
Cavernous haemangiomas
These consist of dilated, thin-walled, blood-filled vessels or sinusoids covered
by squamous epithelium (Fig. 211). If a haemangioma needs to be removed,
cryotherapy is probably then the treatment of choice because of the risk of
serious haemorrhage.
Soft tissue haemangiomas usually only require excision if a source of frequent

bleeding secondary to trauma. Cryotherapy may lessen bleeding.
Intraosseous haemangiomas have rarely led to fatal haemorrhage when opened

accidentally. Large high- flow intraosseus haemangiomas require embolization
of feeder vessels before excision.
Fig. 209 Plexiform neurofibroma.
Fig. 210 Capillary haemagioma.
Fig. 211 Cavernous haemangioma.120 Microscopy
Microscopy
Treatment
Lymphangiomas
Generally resemble cavernous haemangiomas but consist of dilated lymphatic

vessels which do not contain blood cells unless traumatized (Fig. 212).
Large, disfiguring lymphangiomas may require excision but this may be difficult
because of the problem of defining their margins.
Vascular leiomyomas
These are rare, benign tumours of smooth muscle of vessel walls. They consist
predominantly of smooth muscle cells which are concentrically arranged around
small vessels but spread out without any regular pattern into the main tumour
areas. The smooth muscle cells are not obvious in H & E stained sections but are
made conspicuous with special stains such as PTAH (Fig. 213).
Leiomyomas respond to complete excision. Lipoma

Lipomas are benign tumours of fat cells and most commonly arise from the
buccal fat pad.
The mass consists of fat cells (adipocytes) held together by loose areolar tissue
and covered by mucosa (Fig. 214). Excision is curative.
Liposarcomas
These are recognized but exceedingly rare oral tumours.
Wide excision is the treatment of choice but recurrence is common. The extent
of the neoplasm and the histological type affect the outcome.
Fig. 222 Lymphangioma.
Fig. 213 Vascular leiomyoma. (PATH stain.)
Fig. 214 Lipoma.122
Chapter-17
Sarcomas
Microscopy
Prognosis
Kaposi’s sarcoma
As a result of the worldwide spread of HIV infection, the previously rare

Kaposi’s sarcoma has become one of the most common types of sarcoma and is
the most common oral tumour in AIDS. In HIV infection, Kaposi’s sarcoma is
most frequent in male homosexuals. It can also complicate deep
immunosuppression but mainly in those who are HLA B5. In these conditions,
Kaposi’s sarcoma frequently appears in the mouth as a purplish plaque or
nodule.
The tumour is thought to be of viral origin, probably HHV8, and secondary to

the immunodeficiency state.
Kaposi’s sarcoma is a tumour of endothelial cells (as shown by the marker for
factor VIII) but these largely assume a spindle shape (Fig. 215). Early lesions
consist of proliferating capillaries, usually with many inflammatory cells, and
closely resemble granulation tissue.
Later there are fibrosarcoma-like interlacing bands of spindle-shaped tumour

cells surrounding slit-like vessel lumens or minute round lumens when cut in
cross-section (Fig. 216). The inflammatory element progressively disappears, the
tumour cells become more pleomorphic and mitoses become numerous (Fig.
217). Interspersed are haemangioma-like areas with more obvious vascular
spaces.
Kaposi’s sarcoma has a poor prognosis in AIDS and is usually fatal within 2
years of diagnosis, if treatment fails. However, associated infections secondary
to the immunodeficiency are more frequently the cause of death.
Fig. 215 Kaposi’s sarcoma: proliferating endothelial cells and slit-like vascular spaces.
Fig. 216 Kaposi’s sarcoma: spindle cells and trans- versely cut vascular spaces.
Fig. 217 Kaposi’s sarcoma: mitotic activity.124 Microscopy

Microscopy
Prognosis
Microscopy
Fibrosarcoma
Oral fibrosarcomas are exceptionally rare. The peak age incidence is between 35
and 55. They form firm swellings without distinctive clinical features.
Malignant fibroblasts form dense interlacing bundles of uniform, elongated,

spindle-shaped cells with occasional mitoses and some collagen formation. With
increasing dedifferentiation the arrangement of the cells becomes more irregular,
mitoses become more frequent and less collagen is produced (Fig. 218).
Metastases may develop many years after diagnosis and usually form in the
lungs.
Rhabdomyosarcoma
Rhabdomyosarcomas are also rare but the most common type of oral sarcoma in
children.
The alveolar type shows spindle-shaped spaces from the walls of which hang
round or pear-shaped, darkly staining cells (Fig. 219).
Embryonal rhabdomyosarcomas are highly pleomorphic and consist of a loose,

unorganized mass of cells without obviously identifiable features (Fig. 220)
unless cross-striations are seen; immunocytochemistry for muscle cell markers is
helpful.
Rhabdomyosarcomas are highly malignant. Radical excision followed by

radiotherapy and/or chemotherapy is the usual treatment but there is frequently
local recurrence or distant metastases. The lungs or bones are the main sites of
metastases but lymph nodes may be involved in about 50%: death may follow in
1–6 years.
Rhabdomyoma
The main site for this rare tumour is the tongue.
Large, round, granular eosinophilic cells contain large amounts of glycogen and,
frequently, fat spaces. Cross-striations may be seen (Fig. 221) or may be
demonstrable only by special stains.
Rhabdomyomas are benign.

Fig. 218 Fibrosarcoma.
Fig. 220 Rhabdomyosarcoma: pleomorphic type.
Fig. 219 Rhabdomyosarcoma: alveolar cell type.
Fig. 221 Rhabdomyoma of tongue.126
Chapter-18
Lymphomas
Microscopy
Lymphomas comprise Hodgkin’s disease and nonHodgkin’s lymphoma. Non-

Hodgkin’s lymphoma usually arises from B lymphocytes and the different
variants result from the stage of development of the lymphocyte undergoing
neoplastic change The cell of origin of Hodgkin’s disease is uncertain but may
be the monocyte or T lymphocyte.
Lymphomas (particularly Hodgkin’s disease) are rare in the mouth, far more
commonly affecting cervical lymph nodes, but are considerably more frequently
seen in patients with AIDS. In the mouth they may be the primary lesion or the
presenting feature of disseminated disease.
Lymphomas are one of the most difficult areas of histopathology, as reflected by

the many classifications. The essential feature is proliferation of lymphocytes
either diffusely (Fig. 222) or with a follicular pattern According to the type, the
lymphocytes range from large immature lymphoblasts to small mature cells or
immunoblasts (Fig. 224). Monoclonal immunoglobulin production may be
detected. Surrounding tissues may be invaded (Fig. 223). Hodgkin’s disease is
remarkable for the variety of cells present, including lymphocytes, histiocytes,
eosinophils and Reed–Sternberg cells. The latter are large cells with a
symmetrical (mirror-image) pair of large vesiculated nuclei.
The prognosis of non-Hodgkin’s lymphoma varies according to the histological

type and particularly to the stage of development when detected. If reasonably
localized, Hodgkin’s disease responds to radiotherapy and/ or chemotherapy.
Fig. 222 Lymphocytic lymphoma.
Fig. 223 Lymphoma invading muscle.
Fig. 224 Immunoblastic lymphoma.128 Chapter-19
Pigmented Lesions
Microscopy
Microscopy
Prognosis 129
Pigmented naevi
These range from bluish-brown macules resembling amalgam tattoos to

extensive black areas, usually on the palate.
The pigment cells (melanocytes) can be intradermal (in the submucosal

connective tissue) (Fig. 225), or junctional (clusters of melanocytes projecting
from the epitheliomesenchymal junction into the underlying corium) (Fig. 226),
appearing to drop down from the epithelium. In adults junctional activity is
suggestive of malignant melanoma. Compound naevi show a combination of
both features.
Naevi are benign but all oral pigmented lesions should undergo excision biopsy
to exclude malignant melanoma.
Malignant melanoma
Oral malignant melanomas are rare, are often large before being noticed and the
prognosis is therefore poor. Amelanotic melanomas appear as reddish areas or
nodules. Peak incidence is at 40–60 years.
The features can include:
intraepithelial melanocytes, typically with clear halos round them

junctional activity with melanocytes in large, clear areas within and dropping
from the basal layer
proliferation of melanocytes in the submucosal connective tissue.
Malignant melanocytes range from round to spindle- shaped and can be in solid
sheets, rounded, circumscribed groups or in fascicles (Fig 227 and Figs 228–229,
p 132). Pigment may be dense or invisible without special staining.
Wide excision followed by radiotherapy is the usual treatment but the 5-year
survival rate of oral melanomas is only about 25%.
Fig. 225 Melanocytic naevus.
Fig. 226 Junctional activity and pigmentation.
Fig. 227 Malignant melanoma: pigmented melano130 cytes.
Amalgam tattoo
Clinically, amalgam tattoos are by far the most common oral pigmented lesions.
Histologically, the amalgam is seen as black particles or larger masses lying in
the connective tissue, frequently with no foreign body reaction (Fig. 230).
Biopsy is usually required to exclude an early melanoma.
Fig. 228 Melanoma. Predominantly spindle-shaped melanocytes with variable pigmentation.

Fig. 229 Melanoma. Spindle-shaped and rounded, heavily pigmented, neoplastic melanocytes.
Fig. 230 Amalgam tattoo. 132 Chapter-20
Miscellaneous Tumour-like Lesions
Microscopy
Prognosis
Granular cell tumour
Clinical appearances are variable; the tumour is usually seen on the dorsum of
the tongue. Adults between the ages of 30–60 years are affected.
Two characteristic features are;
pseudoepitheliomatous hyperplasia of the overlying epithelium (Fig. 231)

granular cells replacing muscle fibres (Figs 232 & 233). The epithelium may
closely resemble carcinoma but
lacks cellular atypia. Cells with coarse eosinophilic granules appear to merge
with muscle fibres. Positive staining for S-100 protein and neurone specific
enolase suggest a neural origin.
Granular cell tumours are benign and respond to excision.

Microscopy
Prognosis
Granular cell epulis of the newborn (congenital epulis)

This soft, rounded swelling may rarely be found on the alveolar ridge of
neonates. The upper jaw is usually affected and most are in female infants.
Close-packed granular cells have prominent cell membranes. The granular cells
stain with myogenic markers (e.g. myosin and actin) but not for S-100 protein.
The overlying epithelium is flat and lacks pseudoepitheliomatous hyperplasia.
The granular cell epulis is benign and responds to excision.
Fig. 231 Granular cell tumour: pseudo-epitheliomatous hyperplasia.
Fig. 232 Granular cell tumour: pseudoepitheliomatous hyperplasia with cell nests and granular tumour cells
beneath.
Fig. 233 Granular cell tumour: granular tumour cells 134 merging with muscle fibres.
Chapter-21 Salivary Gland Tumours
Pleomorphic adenoma
This is the most common type of salivary neoplasm but forms only about 40% of
intra-oral salivary gland tumours. Typical intraoral sites are palate, lip and buccal
glands.
Microscopy Pleomorphic adenomas form from epithelial and myoepithelial

cells. Myoepithelial cells cannot be reliably recognized by light microscopy but
appear as spindle-shaped, hyaline (plasmacytoid) or clear cells. They can be
identified by immunostainmg positively with both epithelial and muscle cell
markers. Myoepithelial cells produce the connective tissue structures in
pleomorphic adenomas as a result of their multipotential properties.
Highly variable patterns are seen even within individual tumours (Fig. 234).
Common features include: duct-like structures (Fig. 235)
sheets of small, dark epithelial cells
squamous metaplasia and keratin formation (Fig. 236) basophilic mucoid areas,
sometimes forming the bulk
of the tumour (Fig. 237)

cartilage (see Fig. 238, p. 138) and, occasionally, bone fibroblast like
myoepithelial spindle cells ‘plasmacytoid’ hyaline myoepithelial cells (see Fig.
239, p 138).
Fig. 234 Pleomorphic adenoma: typical mixed pattern.
Fig. 236 Pleomorphic adenoma squamous metaplasia.
Fig. 235 Pleomorphic adenoma: tubular structures.
Fig. 237 Pleomorphic adenoma: myxoid type.136 Prognosis
Treatment
Pleomorphic adenoma (2)
There is a fibrous capsule, but it is frequently incomplete and tumour often

extends through the capsule without invading surrounding tissues (Fig. 240).
Pleomorphic adenoma is slow growing and benign but can undergo malignant
change (see p. 143; Carcinoma in pleomorphic adenoma), usually after many
years. Carcinoma may then be seen adjacent to typical pleomorphic adenoma
components in the same tumour.
Complete excision is essential and curative. Incomplete excision typically leads

to multinodular growth and increased risk of malignant change. Recurrence of
pleomorphic adenomas results from:
surgical difficulties of removal, especially from the parotid gland
extension of the tumour through the capsule seeding of spilt tumour cells into
the incision (due to attempted enucleation), leading to multinodular recurrences
(Fig. 241). Pleomorphic adenomas are not initially multinodular.
Fig. 238 Pleomorphic adenoma: cartilage with calcification.
Fig. 240 Pleomorphic adenoma: infiltrating the capsule.
Fig. 239 Pleomorphic adenoma: hyaline cells.
Fig. 241 Pleomorphic adenoma: seedlings from 138 failed enucleation.
Microscopy
Prognosis
Monomorphic adenomas
These have a uniform pattern often of trabecular or canalicular pattern (Figs 242
& 243) and lack the connective tissue components of pleomorphic adenoma.
There are several subtypes.
Warthin’s tumour (Adenolymphoma)
Warthin’s tumours form about 10% of salivary gland tumours but virtually all
are in the parotid gland and about 5% are bilateral. Intra-oral glands are probably
never affected. This tumour is mostly seen in middle age and typically forms a
soft or cyst-like mass in the lower pole of the parotid.
The two components are glandular epithelium and lymphoid tissue (Fig. 244).
Tall, columnar, eosinophilic epithelial cells (Fig. 245) surround and protrude into
cystic spaces and cover lymphoid tissue consisting of small lymphocytes and,
usually, germinal centres. The tumour is benign.
Monomorphic adenomas, including Warthin’s tumour, are benign and have less
tendency to recur after excision than pleomorphic adenomas.
Fig. 242 Monomorphic adenoma.
Fig. 244 Warthin’s tumour.
Fig. 243 Canalicular monomorphic adenoma of lip.
Fig. 245 Warthin’s tumour: epithelial component.140 Microscopy
Prognosis
Microscopy
Prognosis
Mucoepidermoid carcinoma
Mucoepidermoid carcinoma can be relatively benign or can behave like a typical

carcinoma. It forms nearly 10% of intra-oral salivary gland tumours; most
commonly on the palate. Patients are usually middle-aged or older.
The two components are large, pale, mucus-secreting cells, which typically
surround large or small cystic spaces (Figs 246 & 247), and sheets of epidermoid
cells. Less well differentiated tumours tend to resemble squamous cell
carcinomas but for the presence of occasional mucous cells (Fig. 248).
Behaviour of mucoepidermoid carcinomas is not reliably predictable from

histological appearances. They can be invasive and metastasize even when
cytologically benign (Fig. 247). Wide excision is therefore required.
Acinic cell carcinoma

Forms only about 2% of intra-oral salivary gland tumours.
Typically a more or less uniform pattern of large, darkly basophilic cells with
granular cytoplasm (Fig. 249) resembling serous acinar cells. Often tumour cells
are in sheets without obvious organization but occasionally in an acinar
arrangement.
Acinic cell carcinomas even when cytologically benign can also be invasive and
metastasize. Wide excision is therefore required.
Fig. 246 Mucoepidermoid carcinoma.
Fig. 248 Mucoepidermoid carcinoma: epidermoid and mucous cells.
Fig. 247 Mucoepidermoid carcinoma invading bone.
Fig. 249 Acinic cell carcinoma.142
Microscopy
Microscopy
Microscopy
Adenoid cystic carcinoma

Forms 13% of intra-oral salivary gland tumours.
Typically consists of small, dark cells with duct-like ‘holes’ in a cribriform

(Swiss cheese) (Fig. 250) or lace-like pattern, often with hyaline or mucinous
change in the stroma. It has a strong tendency to perineural invasion (Fig. 251)
and spread.
The tumour is slow-growing but difficult to excise as the borders are ill-defined.
Metastases develop late and radical excision is needed.
Adenocarcinoma and other carcinomas Form about 12% of intra-oral salivary

gland tumours, and mainly affect the over 60s.
Well-differentiated tumours form glandular patterns (Fig. 252) or cysts with

papillary ingrowths. Less-welldifferentiated tumours show greater cellular
pleomorphism.
Undifferentiated carcinomas and squamous cell carcinomas are rare and seen
mostly in the elderly.
Carcinoma in pleomorphic adenoma
Pleomorphic adenoma can undergo malignant change, usually after years of slow
growth, in recurrences and in old fibrotic (scarred) tumours (Fig. 253).
Carcinoma in pleomorphic adenoma comprises about 7% of salivary tumours of
minor glands but up to 30% of sublingual gland tumours.
Malignant change is usually adenocarcinoma (Fig. 253) or undifferentiated

carcinoma with invasion and destruction of surrounding structures, but
elsewhere features of original pleomorphic adenoma persist.
Fig. 250 Adenoid cystic carcinoma.
Fig. 252 Adenocarcinoma.
Fig. 251 Adenoid cystic carcinoma: perineural invasion.
Fig. 253 Carcinoma in pleomorphic adenoma.144
Chapter-22
Salivary Gland Cysts and Chronic Non-specific Sialadenitis
Aetiology
Prognosis
Salivary gland cysts (mucoceles)
Mucous extravasation cysts
Most common type of soft tissue cyst. Minor glands, especially of the lip, are
affected.
Probably mainly result from injury to the duct, leading to leakage and formation
of pools of saliva in overlying soft tissues with inflammatory reaction (Fig. 254).
Coalescence of pools of saliva leads to the formation of a cyst with lining of
fibroblasts and compressed fibrous tissue (Figs 255 & 256).
Salivary retention cysts
Rare variant of mucocele produced by duct obstruction, forming a clinically
similar lesion but the cyst is lined by flattened duct epithelium (Fig. 257).
Mucoceles respond to simple excision but the damaged gland must also be
removed to prevent recurrence.
Aetiology
Microscopy
Prognosis
Chronic non-specific sialadenitis
Commonly a consequence of obstruction to salivary secretion, sometimes in

association with calculus formation.
Scattered, mainly periductal infiltration by chronic inflammatory cells, dilatation

of ducts, degeneration of acini and increasing fibrous replacement (see Fig. 258,
p.148) are the characteristic features.
Chronically inflamed glands do not resolve spontaneously and need to be

removed to exclude a tumour as the cause of the swelling.
Fig. 254 Extravasation mucocele and attached salivary tissue.
Fig. 256 Extravasation mucocele: fibrous wall.
Fig. 255 Extravasation mucocele: connective tissue wall (above); mucin-and-lipid laden macrophages in
contents.
Fig. 258 Salivary mucous retention cyst: epithelial 146 lining.
Microscopy
Prognosis
Salivary calculi
Calculi form usually by concretion of calcium salts round a nidus of organic

matter, particularly in the submandibular gland. Calculi may be multiple within
the gland or solitary and in the duct. Sialadenitis with duct dilatation is typically
associated.
Calculi appear either as lamellated structures or multiple concretions which fuse

to form a single mass. The surrounding duct epithelium may undergo squamous
metaplasia (Fig. 259) and the surrounding tissue may be inflamed.
Calculi need to be removed as obstruction of the duct predisposes to infection of

the gland.
Microscopy
Prognosis
Sjögren syndrome and related disorders
Sjögren syndrome comprises dry mouth, dry eyes and connective tissue disease
—usually rheumatoid arthritis. Sicca syndrome has no associated connective
tissue disease and differs in the immunological findings. Salivary
lymphoepithelial lesion is the same histologically as Sjögren syndrome. These
conditions mainly affect women, usually over 50.
Infiltration of salivary tissue by lymphocytes and plasma cells is initially

periductal (Fig. 260). The infiltrate spreads outwards and leads to progressive
destruction of acini but ducts are more resistant (Fig. 261). Eventually, only
lymphoplasmacytic cells and islands of hyperplastic duct epithelium
(‘epimyoepithelial islands’) may remain. The lymphoplasmacytic infiltrate
remains confined within the salivary lobules and does not penetrate the gland
septa.
Labial salivary glands show close correlation with the parotid changes, but
epimyoepithelial islands are rare.
There is no curative treatment and lymphomatous change is a hazard.

Symptomatic treatment is needed for xerostomia and xerophthalmia.
Fig. 258 Non-specific sialadenitis.
Fig. 260 Sjögren syndrome: early stage.
Fig. 259 Salivary calculi: dquamouaplasia of duct lining.
Fig. 261 Sjögren syndrome: destruction of gland 148 acini, and epimyoepithelial islands.
Chapter-23
Granulomatous Diseases
Aetiology
Microscopy
Prognosis
Microscopy
Prognosis
149
Histologically, granulomas are focal, rounded collections of macrophages, often

with giant cells, as in tuberculosis. Clinically, however, ‘granuloma’ is used for
many chronic inflammatory conditions (e.g. apical granuloma, etc.) which lack
granulomas histologically.
Tuberculosis
Tuberculous oral ulceration, secondary to chest infection, is occasionally seen in

AIDS patients, otherwise very rare. Mycobacteria are rarely found in oral lesions
but are present in sputum.
Deep ulcer with overhanging edges (usually on dorsum of tongue) with

tuberculous granulomas and Langhans’ giant cells (Figs 262 & 263).
Response depends on clearing the pulmonary infection. In AIDS patients the

prognosis of mycobacterial infections is poor due to multiply resistant bacteria.
In the absence of HIV infection, tuberculosis usually responds to multiagent
chemotherapy.
Fungal infections (systemic mycoses)
Immunosuppressed and AIDS patients are susceptible to many fungal infections

such as histoplasmosis or aspergillosis. Other such infections are common in
South America. Many produce oral lesions at some stage.
Several of the mycoses ( not candidosis) produce granulomatous reactions more

or less resembling tuberculosis (Fig. 264). Tissue forms of the fungus, usually
spore forms or hyphae, may sometimes be detectable, but usually only with
special stains. Histoplasma capsulatum is unusual in that the spores, with
characteristic halo-like capsule, may be seen in H & E stained sections (Fig.
265).
Treatment with amphotericin or an imidazole antifungal drug is likely to be

effective unless infection is too widespread.
Fig. 262 Tuberculous ulcer of lip edge.
Fig. 264 Histoplasmosis of the tongue: Langhans giant cell and granuloma.
Fig. 263 Tuberculous granuloma beneath ulcer.
Fig. 265 Histoplasma capsulatum: spores sur150 rounded by halo-like capsule.
Microscopy
Prognosis
Actinomycosis
Neither a mycosis nor a granulomatous disease histologically. Clinically,

actinomycosis most frequently affects the soft tissues at the angle of the jaw, but
only exceptionally rarely involves bone The causative organism is usually
Actinomyces israelii, a filamentous bacterium found in normal mouths. The
reason for its occasional invasion of tissues in the immunocompetent person is
unknown, but it is now increasingly rarely seen.
Actinomyces israelii , if it invades the tissues, produces multiple abscesses.

There is suppuration, with a central colony of filamentous bacteria surrounded
by fibrosis, and sinuses develop (Figs 266 & 267). Inflammatory reaction and
fibrosis typically fail to localize the infection, which, if untreated, spreads
through the tissues producing multiple sinuses. Lymph nodes are not involved
except by direct extension of the infection.
The diagnosis is confirmed by culture of pus, but is unlikely to be positive unless

‘sulphur granules’ (colonies of Actinomyces) are present.
Good response to vigorous, early treatment, usually with penicillin. Surgical

drainage rarely required.
Aetiology
Pathology
Microscopy
Diagnosis
Sarcoidosis
Unknown. Minor immunological defects may be associated—especially negative
reaction to tuberculin.
Hilar lymph nodes and sometimes peripheral lung are the main sites but almost
any tissue can be affected. There is a predilection also for salivary tissue,
especially labial glands. Gingival enlargement develops in some cases.
Compact histiocytic granulomas without caseation, often multiple and with giant
cells
(Fig. 268)
.
Diagnosis is usually dependent on combined laboratory and clinical findings, in

particular, evidence of pulmonary involvement, biopsy of affected tissue,
positive Kveim test or raised serum angiotensin converting enzyme (ACE)
levels.
151
Fig. 266 Actinomycosis: loculus with central colony surrounded by neutrophils and fibrous abscess
wall.
Fig. 267 Actinomycosis: detail of bacterial colony.
Fig. 268 Sarcoidosis: typical granuloma with giant 152 cell.
Prognosis
Microscopy
Prognosis
153
Sarcoidosis (cont’d)
Heerfordt syndrome comprises swelling of the parotid glands, xerostomia,
uveitis and facial palsy.
Intralesional corticosteroids are sometimes given for troublesome oral lesions.

Pulmonary fibrosis or hypercalcaemia are the main complications for which
systemic corticosteroids are required.
Crohn’s disease
Aetiology unknown. Typically there is intestinal (particularly ileocaecal)

granulomatous inflammation, causing ulceration, fibrosis and thickening of the
intestinal wall and bowel dysfunction (diarrhoea and/or constipation and pain).
Complications include malabsorption leading to vitamin deficiencies.
Oral lesions consist of soft mucosal thickenings causing a cobblestone

appearance, mucosal tags or ulceration.
Subepithelial oedema, chronic inflammation and granulomas which are typically

loose-textured, scattered and sometimes present only deeply (Figs 269 & 270).
Investigation is required for bowel symptoms which may respond to

sulphasalazine or its analogues but response is variable. Oral lesions sometimes
respond to sulphasalazine.
Melkersson Rosenthal syndrome
Characterized by facial or labial swelling, recurrent facial palsy and fissured

tongue. Unknown aetiology. Shows granulomas in the affected tissues.
Orofacial granulomatosis
This term is used for granulomatous lesions clinically and histologically

resembling those of Crohn’s disease or sarcoidosis but without any other features
of such diseases. Some of these reactions appear to be due to food additives and
occasionally respond to restriction diets. In others, manifestations of sarcoidosis
or Crohn’s disease may appear later (Fig. 271).
Fig. 269 Crohn’s disease of oral mucosa.
Fig. 270 Crohn’s disease: a mucosal tag containing granulomas.
Fig. 271 Orofacial granulomatosis. Similar granulo154 mas to Crohn’s disease in the absence of
systemic disease.
Microscopy
Microscopy
Prognosis
Midline granuloma syndrome (lethal midline granuloma)

These rare syndromes have initial nasopharyngeal symptoms leading to
midfacial destruction of tissues and a fatal termination. In the past, similar
appearances could be produced by such diseases as tuberculosis, syphilis or
systemic mycoses, but these are separate and treatable entities. The main causes
of midline granuloma are now Wegener’s granulomatosis and peripheral T-cell
lymphomas.
Wegener’s granulomatosis
Typically comprises granulomatous nasal inflammation, pulmonary and renal
involvement, plus, occasionally, a characteristic proliferative gingivitis
(‘strawberry gums’) or, later, mucosal ulceration.
There is necrotizing arteritis with giant cells (Fig. 272) scattered or related to the
inflamed vessels. The giant cells may be small with few nuclei or resemble
Langhans cells. Granulomas are a characteristic feature but may be difficult to
see in a dense inflammatory infiltrate.
Gingival biopsy showing giant cells may allow early successful cytotoxic
treatment. Otherwise renal involvement can be fatal.
Nasopharyngeal T-cell lymphomas
Nasopharyngeal T-cell lymphomas can produce initial symptoms
indistinguishable from Wegener’s granulomatosis but, occasionally, extension of
tissue destruction produces palatal perforation and ulceration (Fig. 273).
The cellular picture is highly pleomorphic but the lymphoma cells can surround,
infiltrate and destroy blood vessels and so closely mimic true (inflammatory)
vasculitis.
Ultimately systemic spread is like that of other lymphomas but may be slow.
Early cytotoxic treatment and/or radiotherapy may be effective.
Fig. 272 Wegener’s granulomatosis: typical giant cells in gingival biopsy.
Fig. 273 Nasopharyngeal T-cell lymphoma: neoplastic lymphocytes surrounding and destroying an
arteriole.156
Chapter-24
Miscellaneous Fibrotic Conditions
Aetiology
Microscopy
Prognosis
Progressive systemic sclerosis (scleroderma)
A connective tissue (autoimmune) disease producing progressive fibrosis and

stiffening of the skin and viscera. Limitation of opening of the mouth and
movement of the tongue and Sjögren syndrome may develop Antmuclear bodies
are present.
Progressive fibrous thickening of submucosa extending into and destroying

superficial muscle fibres. There is a perivascular lymphocytic infiltrate (Fig.
274).
The 5-year survival rate is only about 50% due to visceral or pulmonary disease.
Aetiology
Microscopy
Prognosis
Oral submucous fibrosis
Affects those from the Indian subcontinent and may be related to Areca nut
chewing, but the aetiology is uncertain. It is not an autoimmune condition. There
is intense, symmetrical, thick board like stiffening of sites such as the palate,
cheeks or lip, but not of the viscera or other parts of the body.
Similar to scleroderma but more intense and lacking perivascular infiltrate (Fig.
275). Sometimes there is epithelial dysplasia, which is possibly premalignant.
Oral submucous fibrosis is disabling when it becomes impossible to open the

mouth adequately. There is also a risk of carcinomatous change.
Fig. 274 Scleroderma: submucosal fibrosis with muscle destruction in the tongue and perivascular

lymphocytic infiltrate.
Fig. 275 Oral submucous fibrosis: deeper extension of fibrosis and muscle destruction than in
scleroderma.158
Chapter-25
HIV Infection and AIDS
Microscopy
Prognosis
Human immunodeficiency virus (HIV) particularly infects and destroys T helper

(CD4) lymphocytes, leading (usually) to progressively more severe defects,
particularly of cell-mediated immunity and, eventually, gross immunodeficiency.
Death is usually due to opportunistic infections but lymphomas and Kaposi’s
sarcoma (see p. 123) are also common. CNS cells are also directly involved and
cranial nerve lesions may result.
‘Hairy’ leukoplakia
Usually painless, soft, white plaque with corrugated surface along lateral borders
of the tongue. Hair-like protrusions of keratin are rarely seen.
Hyperkeratosis with ridged surface (Fig. 276); often colonized by C. albicans or
bacteria A zone of koilocytes (vacuolated and ballooned prickle cells with
pyknotic nuclei) is seen in the prickle cell layer (Fig. 277). Epstein-Barr virus
capsid antigen is identifiable in the nuclei (Fig. 278).
There is no evidence of malignant potential but over 80% of these patients

develop AIDS within 3 years.
Other typical oral manifestations

Candidosis (any type)
HIV gingivitis or periodontitis
Necrotizing ulcerative gingivitis
Kaposi’s sarcoma and lymphomas Less frequent are: atypical ulcerations
lymphoepithelial lesions of salivary glands
infections by herpes simplex or varicella-zoster, cytomegalovirus or human

papillomavirus
deep mycoses.
See preceding pages for the pathology of these lesions.
Fig. 276 Hairy leukoplakia in HIV infection: ridged hyperkeratotic surface, acanthosis and scanty
inflammatory infiltrate beneath.
Fig. 277 Hairy leukoplakia: hyperplastic epithelium
with koilocytes beneath the surface.
Fig. 278 Hairy leukoplakia: positive staining for 160 Epstein–Barr virus capsid antigen.
Chapter-26 Additional Information for
Dental Caries
Dead
tracts
Fig. 279 (a) (b) Dead tracts: Dentinal areas characterized by degenerated odontoblastic processes; may
result from injury caused by caries, attrition, erosion or cavity preparation. They appear black in transmitted
light and white in reflected light.
Striae of Retzius
Fig. 280 The Striae of Retzius: They represent the poorly calcified portion of enamel, extending
from the dentino-enamel junction towards the tooth surface. Their meeting point at enamel surface forms
grooves encircling the tooth known as Perikymata.
Leaflike
E
DEJ D
Fig. 281 Enamel lamellae: These are thin, leaflike structures that extend from the enamel surface
towards the DEJ; rarely extending into dentin. The lamellae consist of organic material with little mineral
content.
Fig. 282 Longitudinal ground sections of teeth depicting cemento-enamel junction a. edge to edge relation,
b. gap junction, c. cementum overlapping enamel. (E: Enamel; D: Dentin; C: Cementum).
Dentin
CDJ
Cementum
Fig. 283 Longitudinal ground section of tooth showing cemento-dentinal junction (arrow).
Fig. 284 Longitudinal ground section of tooth depicting zones of enamel caries. 1. Surface zone; 2. Body
of lesion; 3.Dark zone; 4.Translucent zone. (E: Enamel; D: Dentin).
Fig. 285 Longitudinal ground section of tooth depicting zones of dentinal caries. (1) Zone of fatty

degeneration of Tome’s fibers, (2) Zone of dentinal sclerosis, (3) Zone of decalcification, (4)
Zone of 162 bacterial invasion, (5) Zone of decomposed dentin.
Chapter-27 Multiples Choices Questions (MCQs)
1. Union of adjacent teeth through cementum a. Fusion b. Germination c.

Concrescence d. All of the above
2. Deformity of tooth due to sharp bend in the root is a. Fusion

c. Concrescence
3. Teeth that erupt at birth a. Natal teeth

c. Primary teeth b. Germination d. Dilaceration
b. Neonatal teeth d. Prenatal teeth
4. Developmental anomaly with less than usual number of teeth is a. Anodontia

c. Microdontia
5. Anodontia affects the growth of a. Mandible

c. Alveolar bone
6. Ghost teeth are seen in
a. Regional odontodysplasia c. melogenesis imperfecta
7. Turners tooth occurs due to a. Trauma of infection c. Birth injuries

b. Oligodontia d. Dens in dente
b. Maxilla d. Cranium
b. d. Craniofacial dysostosis None of the above
b. d. Syphilis
Hypercalcemia
8. Most common supernumerary tooth form is

a. Conical b. Screw shaped c. Tuberculated d. Incisor form
9. Hutchinson’s incisors are seen in which stage of syphilis?? a. Primary b.

Secondary c. Tertiary d. Congenital
10. Talon’s cusp is associated with

a. Edward’s syndrome b. Down’s syndrome c. Klinefelter’s syndrome d.
Rubinstein-Taybi syndrome
11. Bilateral mandibular enlargement is seen in:

a. Cherubism b. Fibrous dysplasia c. Paget’s disease d. CGCG
12. Osteosarcoma can arise from:
163 a. Paget disease and Cherubism

b. Cherubism and Osteopetrosis
c. Paget disease and polyostotic fibrous dysplasia
d. Polyostotic fibrous dysplasia and Cherubism
13. Among Hepatitis –A, Syphilitic glossitis, Plummer Vinson syndrome,
Mikulicz’s syndrome, squamous cell carcinoma is most likely to occur in: a.

Syphilitic glossitis and Plummer Vinson syndrome
b. Syphilitic glossitis and Mikulicz’s disease
c. Plummer Vinson disease and Hepatitis-A
d. Hepatitis-A and Mikulicz’s disease
14. Condition which is unusual to have gingival involvement:
a. Pyogenic granuloma b. Primary herpes
c. Pemphigoid d. Recurrent aphthae
15. Disposal of yellow bag material in hospital

a. Burial b. Autoclave
c. Incineration d. Recycled
16. Riga fede disease is associated with:

a. Natal teeth b. Multiple impacted teeth c. Permanent incisor d. Primary incisor
17. In a patient with acute pulpitis, it is difficult for the patient to locate the
source of pain in the same arch. This is because:
a. No nociceptors are present in pulp
b. Less proprioceptors are present in pulp
c. Patient is not cooperative
d. Patient cannot understand language
18. Which of the following is most common cyst associated with adjoining vital
teeth:
a. Dentigerous cyst c. Lateral cyst
b. Globulomaxillary cyst d. Periapical cyst
19. A 40 year old lady presents with ameloblastoma in mandibular molar region.
Histopathology reveals:
a. Peripheral pallisading cellular strands with central loose stellate
reticulum
b. Peripheral pallisading with central stromal retraction artifact c. Nests, strands,
cords of epithelium in fibrous connective tissue
stroma
d. Central loose stellate reticulum shows marked nuclear atypia
20. Which of the following is true microdontia of lateral incisor? a. Peg lateral b.
Hutchinson’s teeth c. Cheesy teeth d. Mulberry molars
21. A child having extra X chromosome exhibits:

a. Dilacerations c. Impacted teeth b. Dens evaginatus164 d. Taurodontism
22. Facial cleft occurs due to:
a. Failure of ectodermal processes to fuse in midline b. Failure of mesodermal
process to overgrow ectodermal grooves c. Mesodermal processes covered by
ectoderm on both sides d. Failure of endodermal process to fuse in midline
23. Median rhomboid glossitis is due to:

a. Atrophy of filiform papillae
b. Atrophy of fungiform papillae
c. Non fusion of mesodermal thickening and retraction of tubercular impar
d. Incomplete mucosal development seen in the midline of dorsum of tongue
24. About Enameloma, true is:

a. A malignant tumor
b. A globule of enamel like structure presenting at abnormal site
on tooth
c. True neoplasm of ameloblasts which has not reached complete
maturation
d. A tumor resembling enamel present on gingival
25. Among the following pathologies self inoculation is seen in: a. Bullous
Pemphigoid b. Lichen Planus
c. Human Papilloma virus d. Candidiasis
26. Patients with reduced saliva will show caries rate as
a. More
c. Unaffected
27. Fusion occurs at the level of: a. Enamel
c. Cementum
b. Less
d. None of the above
b. Dentine
d. None of these
28. Shell teeth are more common with which variant of dentinogenesis
imperfecta ?
a. Type I b. c. Type III d.
29. Hypodontia is found in all, except a. Papillon Levefre syndrome b. c.

Cleidocranial dysostosis d. Type II
Type I and III
Albers Schonberg disease Ectodermal dysplasia
30. Linear enamel caries lesions in deciduous teeth predominate in: a. Maxillary
exterior teeth b. Maxillary posterior teeth c. Mandibular posterior teeth d.
Mandibular anterior teeth
31. Zone 4 in dentinal caries progression is

165
a. Transparent zone c. Turbid zone b. Subtransparent zone d. Infected dentin

zone 32. Radiographic changes seen in acute osteomyelitis:
a. Mottled appearance c. No change

b. Moth eaten appearance d. Sub burst appearance
33. One of these is a maxilla-nasal dysplasia:

a. Pierre robin syndrome b. Klinefelter syndrome c. Binder syndrome d. Papillon
Levefre syndrome
34. Franceschetti syndrome is:

a. Treacher Collin syndrome b. Vander Woude syndrome c. Fragile X syndrome
d. Williams syndrome
35. Not a feature of Esalante’s syndrome:

a. Macro-orchidism b. Flat feet
c. Narrow face d. Small ears
36. Shredded flag appearance on OPG is shown by:

a. Osteosarcoma b. Osteochondroma c. Fibrous dysplasia d. Osteopetrosis
37. Brainstem syndrome is a component of:

a. Behcet’s syndrome c. SJ syndrome
b. Erythema multiform d. Greenspan syndrome
38. Which of these is termed as ‘thick leukoplakia’:

a. Homogeneous leukoplakia b. Nodular leukoplakia c. Verrucous leukoplakia d.
Proliferative leukoplakia
39. Antigen associated with cicatrical pemphigoid:
a. Laminin-2 b. Lamini-3
c. Laminin-4 d. Laminin-5
40. Witkop syndrome shows which type of inheritance? a. AD b. AR

c. X-linked recessive d. None of these
41. chromosome involved in dentinogenesis imperfecta? a. 2

c. 6
42. Antoni A and B pattern seen in: a. Cellular schwanoma c. Gloms tumor
43. Rain drop pigmentation seen in a. Arsenic poisoning c. Mercury poisoning b.
4 d. 8
b. Neurofibroma d. Melanoma
b. Lead poisoning d. Bismuth poisoning 44. Double teeth is an anomaly most
commonly found in
a. permanent incisors
b. permanent canines 166 c. primary incisors and canines
d. primary molars
45. Enamel hypoplasia is presented with all except

a. Reduction in volume of matrix
b. pits and grooves on the enamel surface
c. enamel with fewer prisms
d. incomplete calcification
46. Hypomineralized enamel characterizes with following except a. Enamel

appears white and opaque
b. tooth may appear pigmented buff, orange, or brownquickly
chipped and worn away

c. organic matrix of hypomineralized enamel remains acid-soluble d. failure of
the ameloblasts to fully calcify
47. Which of the following is an acquired disorder

a. Gemination b. fusion
c. concrescence d. none
48. All of the following are the features seen in congenital syphilis except a.
infection of the tooth germ by spirochaetes
b. Hutchinson’s incisors
c. hypomineralized changes in the enamel
d. Moon’s molars
49. Causes of hypercementosis can be all except:

a. Paget’s disease b. periapical inflammation c. cleidocranial dysplasia d.
mechanical stimulation
50. Transmission of S. mutans occurs mainly through

a. saliva b. skin
c. mother to child d. blood transfusion
51. Which of the following statement is incorrect aboutdental caries a. Caries

prevalence increases when populationsbecome exposed to sucrose-rich diets
b. Intrinsic sugars are more damaging than extrinsicsugars c. Sucrose is the most
cariogenic sugar
d. Frequency of sugar intake is of more importance thantotal
amount consumed
52. Which of the following zone is an area of activeremineralization a. surface
zone c. dark zone b. body of the lesion d. translucent zone
53. Pathological attrition may result from a. excessive intake of acid beverages c.
abnormal occlusion
b. faulty tooth brushing d. habits of pipe smoking
54. Chronic alcoholics may present with the features of 167

a. erosion b. resorption c. abrasion d. attrition
55. It is necessary to avoid the ingestion of tetracyclines between the age groups
from
a. 4months to 7 years b. 1 year to 3 year
c. 4month to 10 month d. 7 month to 5 year
56. Which of the following statement is incorrect aboutpulpitis a. Carbohydrates

is the most important aetiologicalfactor b. dental caries is the commonest cause
c. bacteria can also reach the pulp by other local routes d. trauma to dentine
and/or pulp may cause pulpitisand/or reactionary changes in the pulpodentinal
complex
57. Which of the following cyst arises from glands of Serres
a. dontogenic keratocyst c. radicular cysts
b. dentigerous cysts d. paradental cyst
58. A constant feature associated with radicular cyst is

a. impacted tooth b. missing tooth
c. non vital tooth d. anomalous tooth
59. High recurrence rate of keratocysts is due to all factorsexcept

a. satellite cysts
b. difficulty of surgical removal
c. focal areas of active growth of the cyst wall
d. cystic contents have a low soluble protein level
60. Epstein pearls are

a. same as enamel pearls
b. imperfection in the tooth bud
c. seen in vitamin D deficiency
d. small keratin cysts of newborn infant
61. Cyst resembling the bunch of grapes is

a. Gingival cyst
b. developmental lateral periodontal cyst
c. dentigerous cyst
d. OKC
62. Most cases of pulpitis are caused by

a. injudicious cavity preparation
b. chemical irritation from sterilizing agent
c. bacterial invasion from bloodstream
d. bacterial invasion from carious lesion
63. Which of the following lesion resembles frog’s belly

a. ranula b. Retention mucocele
c. extravasation mucocele d. dermoid cyst
64. Ameloblastic fibroma usually presents in which age groups:168 a. Under 20

years b. Between 20 and 40 years c. Between 40 and 60 years d. Over 60 years
65. While assessing a panoramic xray, you find an asymptomatic multilocular
radiolucency at the body of the mandible in young adult patient. This could be
all the following, EXCEPT:
a. Ameloblastoma
b. Calcifying epithelial odontogenic tumor
c. Odontogenic keratocyst
d. Complex odontoma
e. Odontogenic myxoma
66. Recurrences are least likely seen in which of the following conditions:
a. Ameloblastic fibroma b. Ameloblastoma
c. Odontogenic keratocyst d. Chondrosarcoma
e. Odontogenic myxoma
67. Which of the following conditions appears radiographically as a radiolucent
lesion:
a. Periapical granuloma
c. Odontogenic keratocyst
e. All the above
b. Odontogenic myxoma d. Ameloblastoma
68. Which of the following conditions have high recurrences rate aftercurettage:
a. Dentigerous cyst
b. Adenomatoid odontogenic tumor
c. Nasopalatine duct cyst
d. Complex odontoma
e. Cystic ameloblastoma
69. Which of the following is defined as a clinically benign but aggressive

neoplasm of the jaw iscomposed of epithelium that microscopically mimics
enamel organ:
a. Ossifying fibroma b. Odontoma

c. Ameloblastoma d. Hyperparathyroidism e. Odontogenic myxoma
70. Which of the following lesions is typically seen in middle aged females at
the apices of vital anterior mandibular teeth in
a. Dentigerous cyst
b. Adenomatoid odontogenic tumor
c. Nasopalatine duct cyst
d. Complex odontoma
e. Periapical cemento-osseous dysplasia
71. Which of the following conditions is not known to metastasise from the
jaws: a. Calcifying epithelial odontogenic tumor
b. Ameloblastoma
c. Osteosarcoma
169 d. Ewing’s tumor

e. Chondrosarcoma
72. Which of the following conditions usually present in teenagers, in the

anterior segment of the jaws:
a. Odontogenic myxoma
b. Ameloblastoma
c. Periapical cemento-osseous dysplasia
d. Adenomatoid odontogenic tumor
e. Ameloblastic fibrodontoma
73. While assessing a panoramic xray, you find an asymptomatic 0.5 cm

radiolucent lesion at theapex of tooth no. #45 in you adult female patient. The
pulp tested vital. This lesion is most likely which of the following:
a. Condensing osteitis b. Periapical granuloma c. Periapical scar d. Focal

sclerosing osteitis e. Periapical cemento-osseous dysplasia
74. Which of the following neoplasms microscopically mimics enamel organ: a.

Periapical cemento-osseous dysplasia
b. Odontoma c. Ameloblastoma
d. Ameloblastic fibroma e. Odontogenic myxoma
75. A patient presents with asymptomatic ulcerated erythro-leukoplakia diffusely

affecting the right lateral tongue the preferred technique to take the biopsy in this
situation is
a. Excisional biopsy c. Incisional biopsy b. Punch biopsy d. Brush biopsy
76. Which of the following conditions is least likely to appear in the molarramus
area of themandible: a. Ameloblastoma
c. Myxoma
e. AOT
b. Ameloblastic fibroma d. Chondroma
77. Opaque foci can be seen on x-rays of all the following conditions EXCEPT:
a. CEOT b. Ameloblastic fibroma
c. Myxoma d. Ameloblastoma
e. Cementifying fibroma
78. The best way to reduce the number of deaths due to oral cancer is: a. Take
fewer dental radiographs
b. Relieve all mucosa| irritating aspects of dentures
c. Early detection through oral examination
d. Cytology screening of dental patients
e. Laser surgery
79. A patient shows a radiolucent area surrounding the apices of mandibular

anterior teeth which are vital. The most probable diagnosis is:
a. Periapical granuloma b. Cementoblastoma
c. Radicular cyst d. Myxoma 170 e. Ameoblastoma
80. Marked reduction in amount of dentin, widening of predentin layer, presence

of large areas of interglobular dentin and irregular pattern of dentin is seen in:
a. Hypocalcified dentin b. Odonto dysplasia

c. Dentin dysplasia d. Dentinogenesis Imperfecta
81. A young child presents with a painless, well-defined 1 to 3 cm radiolucent

lesion withradiopaque foci in the posterior. Which of the following should be
included in a differentialdiagnosis:
a. Ameloblastic fibro-odontoma c. Dentigerous cyst

e. Langerhans celldisease b. Paget’s disease d. Ameloblastoma
82. A condition that affects young childrenandis a highly malignant bone tumor,
and most likely to be of a neuro-ectodermal origin is: a. Osteoblastoma c.
Ameloblastoma e. Ewing’s tumor b. Multiplemyeloma d. Brown tumor
83. A young teenage male patient comes to your clinic complaining of numb
lower lip and pain inthe right posterior mandible. A radiograph shows slight
thickening of the periodontal membranespace of tooth #46. The tooth shows
slightly reduced vitality to electric pulp testing. Which of the-following should
be included in a differential diagnosis:
a. Periapical cyst b. Periapical granuloma c. Traumatic bone cyst e. Malignancy
84. Which of the following conditions replaces and is attached to the apices of
teeth:
a. Periapical granuloma
b. Periapical cemento-osseous dysplasia
c. Traumatic bone cyst d. Cementoblastoma
e. Paget’s disease
85. Which of the following benign tumors has been shown to rarely metastasize
to the lungs:
a. Osteoblastoma b. Ameloblastoma
c. Myxoma d. Cementoblastoma
e. Ossifying fibroma
86. All the following is most likely to present in teens and young adults
EXCEPT: a. Traumatic bone cyst c. Fibrous dysplasia e. Garrets osteomyelitis b.
Central giant cell granuloma d. Paget’s disease
87. All of the following characteristically occur in patients under the age of 20
years EXCEPT:
a. Traumatic bone cyst171 c. Ameloblastic fibroma e. Ameloblastoma b. Adenomatoid
odontogenic tumor d. Compound odontoma

88. A circumscribed odontogenic tumor composed of myxofibrous connective
tissue withislands of odontogenic epithelium resembling dental lamina would be

designated as:
a. Ameloblastoma B. Ameloblastic fibroma
c. CEOT d. AOT
e. Calcifying odontogenic cyst
89. A 43-year-old patient developed an asymptomatic 2 to 4 cm enlargement in
the molar-ramusarea. The lesion was well defined, radiolucent, multilocular, and
associated with an impactedtooth. She had no symptoms. Differential diagnosis
could include all the following EXCEPT:
a. Ameloblastoma
b. Calcifying epithelial odontogenic tumor
c. Dentigerous cyst
d. Odontogenic myxoma
e. Adenomatoid odontogenic tumor
90. Which of the following rarely if ever recurs:
a. Calcifying odontogenic cyst b. Ameloblastoma
c. OKC d. Myxoma
e. AOT
91. A radiolucent odontogenic tumor was composed completely of
looseconnective tissue. It had an appearance that had some resemblance to dental
pulp. This is a(n):
a. Ameloblastoma
c. Odontogenic myxoma b. Ameloblastic fibroma d. Complex odontoma e.
Adenomatoid odontogenic tumor
92. A mixed lucent and opaque radiographic pattern may be seen with all the
following jaw lesions except
a. Adenomatoid odontogenic tumor
b. Chronic osteomyelitis
d. Calcifying epithelial odontogenic tumor
e. Ameloblastic fibroma
93. Which of the following is characteristically present in teenagersin the

posterior segment of the jaws
a. Odontogenic myxoma b. Ameloblastoma
d. Ameloblastic fibro-odontoma
e. Calcifying epithelial odontogenic tumor
94. A pear-shaped radiolucency causing displacement of the roots of vital

maxillary lateral and cuspid teeth is characteristics of:
a. Globulomaxillary cyst. c. Primordial cyst.
e. Lateral Periodontal Cyst b. Apical periodontal cyst.172 d. Nasoalveolar cyst
95. Lesion that characteristically occurs on the alveolar ridges of Infants is:
a. Congenital lymphangioma c. Bohn’s nodules

e. Retrocuspid papilla
b. Fordyce granules d. Mite sponge news
96. Features of familial multiple neurofibroma with café-au-lait spots of the skin
are typical of:
a. Von Recklinghausen’s disease of skin
b. Paget’s disease of skin
c. Hereditary ectodermal dysplasia
d. Familial fibrous dysplasia
97. The chemical disintegration of enamel is referred to as:

a. Abrasion b. Attrition
c. Erosion d. Hypoplasia
e. Pitting
98. Mottled enamel is produced by:

a. Syphilis b. Febrile diseases
c. Fluorine d. Acids
e. Tuberculosis
99. The structures of enamel that are more resistant to the actions of acids are: a.
Enamel cuticles
b. Enamel lamellae
c. Enamel rods
d. Interprismatic substance of enamel
e. Ameloblast
100. The most common route by which infection may reach the pulp is through:
a. The blood stream c. Dental caries e. Periosteum
b. Traumatic injuries d. Erosion
101. The cells responsible for root resorption are: a. Fibroblasts c. Osteoblasts e.
Odontoblast
102. Dry socket is a form of a. Osteomyelitis c. Osteoma

e. Granuloma b. Cementoblasts d. Osteoclasts
b. Osteitis d. Periostitis
103. Inflammation of the lips is referred to as: a. Stomatitis 173
c. Cheilitis e. Sialadenitis b. Glossitis migricans d. Vincent Angina 104. Dens In

dente occurs most commonly in the:
a. Maxillary canines
b. Mandibular premolars
c. Mandibular second molars
d. Maxillary lateral incisors
e. All incisors
105. Paralysis of the tongue is referred to as: a. Ankyloglossia

c. Macroglossia
e. Geographic tongue b. Glossoplegia d. Pyroglossia
106. An abnormal disease in the flow of Saliva is called?

a. Ptyalism b. Trismus
c. Xerostomia d. Salivation
e. Sialadenitis
107. The cells most frequently found In a Granuloma are:

a. Mast cells b. Giant cells
c. Lymphocytes d. Neutrophils
e. RBCs
108. A cyst occurring under the tongue, caused by obstruction of a salivary gland
duct, is called a: a. Follicular cyst c. Ranula
e. Epidermoid cyst b. Dentigerous cyst d. Dermoid cyst
109. The most common benign tumor occurring In the oral cavity Is the: a.
Papilloma b. Adenoma
c. Fibroma d. Hemangioma
e. Lipoma
110. The most common malignancy found In the oral cavity is:
a. Basal cell carcinoma
b. Transitional cell carcinoma
c. Melanoma
d. Squamous cell carcinoma
e. Adenocarcinoma
111. The excessive formation of scar tissue is called:

a. Fibroma b. Myxoma
c. Keloid d. Myoma
e. Carcinoma
112. Failure of the tuberculum impar to retract prior to fusion of the lateral
halves of the tongue results In:
a. Median rhomboid glossitis b. Cleft (bifid. tongue174 c. Geographic tongue d. Scrotal
tongue
e. Sarcoma of tongue
113. Atrophy of the pharyngeal and gastric mucosa, koillonychias (spoon nails).
and predisposition to oral carcinoma In postmenopausal women are features of:
a. Iron deficiency anemia

b. Pernicious anemia
c. Sturge-Weber-Dimitri syndrome
d. Plummer-Vinson syndrome
e. Trisomy 21
114. Papillary cystadenoma Lymphomatosum, which occurs almost exclusive
In the parotid gland, Is commonly called:

a. Cylindroma b. Pleomorphic adenoma c. Warthin’s tumor d. Mikulicz disease
e. jaffy’s syndrome
115. A normal clot retraction time, which is independent of coagulation time,
Is indicative of a normal number of circulating:

a. Platelets b. Lymphocytes
c. Monocytes d. Red blood cells
e. Neutrophils
116. The most likely diagnosis in a 23-year-old, mentally alert, male dwarf with
disproportionate arm and log to body growth, prominent forehead, and retruded
maxilla is:
a. Cretinism
c. Acromegaly e. Eagles syndrome b. Pituitary dwarfism d. Achondroplasia
117. Osteosarcoma characteristically may develop in cases of: a. Osteopetrosis c.

Acromegaly e. All of above b. Osteogenesis imperfecta d. Osteitis deformans
118. The blood of a patient with an acute infectious process would be expected
to demonstrate:
a. Lymphocytosis c. Monocytosis e. Erythrocytosis b. Leukocytosis d.
Leukopenia
119. A biopsy would be of value in the diagnosis or oral lesions of a.

Amyloidosis c. Tuberculosis e. All of above b. Carcinoma in situ d. Lichen
planus
120. In an early carious lesions, the first structure to show evidence of

destruction is the:
a. Enamel prism b. Cuticle
175 c. Interprismatic substance d. Lamellae
e. Dead tracts
121. The features of multiple skeletal radiolucencies reversed A/G ratio, Bence
Jones protein in the urine, and solid plasma cell infiltrate In the biopsy In a 50-
year old man indicate a diagnosis of
a. Metastatic prostatic carcinoma

b. Multiple myeloma c. Hyperparathyroidism d. Miliary Tuberculosis e. Basal
cell Navei Syndrome
122. Histiocytosis X, sometimes referred to as non lipid reticulo-endotheliosis,

includes:
a. Letterer-Siwe disease
b. Hand-Schuler-Christian disease
c. Eosinophilic Granuloma
d. Histiocytoma
e. All of above
123. The irradiations to the head region do not cause:

a. Xerostomia
b. Osteoradionecrosis
c. Radiation caries
d. Interference with tooth development
e. Ramsay Hunt syndrome
124. Features of multiple bone radiolucencies, hypercalcemia,

hypophosphatemia, and loss of lamina dura and indicative of:
a. Acromegaly b. Hyperparathyroidism c. Hypothyroidism d. Multiple myeloma
e. Osteitis deformans
125. All the following developmental cysts of the Jaws present as radiolucent
lesions except
a. Median palatal cyst c. Nasoalveolar cyst e. Epidermoid cyst b. Nasopalatine
duct cyst d. Globulomaxillary cyst
126. Koplik’s spots are an early intraoral manifestation of

a. Varicella b. Variola
c. Rubella d. AIDS
e. Mumps
127. Vesicles or bullae of the mucous membrane or skin are seen in all the
following except
a. Herpes simplex c. Agranulocytosis e. SLE
b. Herpes zoster d. Pemphigus
128. White lesion of the oral mucosa are characteristic of the following except a.
Hyperkeratosis b. Leukoedema
c. Lichen Manus d. Medium rhomboid glossitis 176 e. Acanthosis
129. A patient with oral moniliasis that does not respond to nystatin therapy
should be evaluated for the following except

a. Diabetes insipidus b. Diabetes mellitus
c. Hyperparathyroidism d. Malignant lymphoma e. Raised Ca’ in serum
130. The peak incidence of gingivitis in children occurs at ages: a. Birth-6

months b. 1-3 years
c. 5-7 years d. 7-10 years
e. 10-13 years
131. The classic triad of Hand-Schuler-Christian disease includes lesions of

bone, exopthalmous and: a. Diabetes insipidus c. Diabetes mellitus e.
Hypothyroidism b. Hepatosplenomegaly d. Albuminuria
132. Oral cytological smears are of no value in the diagnosis of

a. Oral cancer
b. Primary intraoral herpes simplex
c. Recurrent intraoral herpes simplex
d. Herpes zoster
e. Lipoma
133. The so-called “split papule,” an erosive lesion Involving the commissure of
the lips, Is actually: a. An aphthous ulcer c. A mucous patch e. Koplik’s spot
b. A traumatic ulcer d. A fever blister
134. The stigmata of congenital syphilis does not include: a. Saber shins
c. Eighth nerve deafness e. Cleft lip
b. Interstitial keratitis d. Rhagades
135. Intraoral carcinoma cannot present clinically as:

a. Ulcers
b. Nodule
c. Cauliflower-like growth
d. Growth with fungating margins
e. Abscess
136. The Melkersson-Rosenthal syndrome is characterized by facial paralysis,
Chellitis granulomatosa, and: a. Black Hairy tongue c. Geographic tongue e.

White Hairy tongue b. Scrotal tongue d. Bifid tongue 137. The “Ghon complex
“is associated with:
a. Primary of childhood tuberculosis

b. The adrenogenital syndrome
c. Uveoparotid fever or Heerfordts syndrome
d. Histiocystosis
e. AIDS
138. White, interlacing lines (Striae of Wickham) on the buccal mucosa are a
characteristic clinical feature of: a. Leukoplakia
c. Lichen planus
e. Carcinoma in situ b. Lupus Erythematous d. Psoriasis
139. The most susceptible intraoral site of oral cancer is

a. Floor of mouth
b. Soft palate
c. Attached gingiva & alveolar ridge
d. Lateral borders & ventral surface of the tongue
140. Koplik spots are seen in

a. Measels b. Shingles
c. Herpangina d. Chicken pox
141. Sialoliths are most commonly found in

a. Stensen’s duct b. Wharton’s duct
c. Bartholin’s duct d. Ducts of rivinus
142. A pt.presents with a slow-growing, painless mass at the junction of the soft
and hard palates,which is present for many years without ulceration or
telangiectasia of the overlying mucosa, the most likely diagnosis is
a. Pleomorphic adenoma
b. Monomorphic adenoma
c. Oncocytoma
d. Papillary cystadenoma lymphomatosum
143. A drug induced discoloration is seen in teeth of a child. Which part of the
teeth is affected in this case?
a. Only enamel
b. Only dentin
c. Both enamel & dentin
d. Drugs don’t affect teeth at all
144. A pt.presented with a local abscess with multiple draining sinuses in
Cervicofacial region. The main causative organism most likely is a.

Staphylococci & streptococci b. Oral aerobes
c. Actinomyces israelii d. Enterobacteriaceae
145. Which is responsible for plaque adherence to teeth178 a. Dextrans b. Materia alba
c. Sucrose d. Acquired pellicle

146. The most common pattern of bone loss in periodontal disease is a.
Horizontal bone loss c. Osseous craters
b. Vertical or angular bone loss d. Reversed architecture
147. The primary pathogen associated with localized aggressive periodontitis is

a. Actinomycesactinomycetemcomitans
b. Prevotella intermedia
c. Eikenellacorrodens
d. Campylobacter rectus
148. A female pt.has bilateral reticular white lesion on buccal mucosa,the most
likely diagnosis is
a. Leukoplakia
b. White sponge nevus
c. Reticular lichen planus
d. Mucous membrane pemphigoid
149. Direct immunofluorescence stains reveal a deposit of IgG antibody and C3

in a smooth liner pattern along the basement membrane,the most likely disease is
a. Erosive lichen planus

b. Erythema multiform
c. Bullous pemphigoid
d. Mucous membrane pemphigoid
150. Which of the following induces increased saliva secretions a. Substance P

c. Kallikrein b. Lactoperoxidase d. All of the above
151. A boxer came for extraction of mandibular Ist molar ,the maxillofacial
surgeon was unable to extract the tooth, radiograph shows periapical
radiopacity,the root tip area can be visualized in the bone, most likely he has
a. Hypercementosis b. Periapical granuloma c. Cementoblastoma d.

Concrescence
Answers
1. c 2. d 3. a 4. b 5. c 6. a 7. a
8. a 9. d 10. c 11. a 12. c 13. a 14. d
15. c 16. a 17. b 18. a 19. a 20. a 21. c
22. c 23. d 24. b 25. c 26. a 27. b 28. b
29. b 30. a 31. c 32. c 33. c 34. a 35. d
36. b 37. a 38. a 39. d 40. a 41. c 42. a
43. a 44. c 45. d 46. c 47. c 48. c 49. c
50. c 51. b 52. a 53. c 54. a 55. a 56. a
57. a 58. c 59. d 60. d 61. b 62. d 63. a
64. a 65. d 66. a 67. e 68. e 69. c 70. e
71. a 72. d 73. e 74. c 75. c 76. e 77. d
78. c 79. b 80. b 81. a 82. e 83. e 84. d
85. b 86. d 87. e 88. b 89. e 90. e 91. c
92. e 93. d 94. a 95. c 96. a 97. c 98. c
99. a 100. c 101. c 102. d 103. c 104. d 105. b
106. c 107. c 108. c 109. c 110. d 111. c 112. a
113. d 114. c 115. a 116. d 117. e 118. b 119. e
120. c 121. b 122. e 123. e 124. b 125. c 126. c
127. c 128. d 129. a 130. e 131. a 132. e 133. c
134. e 135. e 136. b 137. a 138. c 139. d 140. a
141. b 142. a 143. c 144. c 145. d 146. a 147. a
148. c 149. d 150. a 151. a
Index
A
Abscess
periodontal, 21, 22
pulp, 7, 8
Acantholysis, 83, 84
Acanthosis, 91, 92
candidosis, 101, 103, 104
cheek-biting, 95
erythema migrans, 97, 98
hairy leukoplakia, 160
leukoedema, 95
Acinic cell carcinoma, 141, 142
Actinomycosis, 151, 152
Acute myelomonorytic leukaemia, 23, 24
Addison’s disease, 103
Adenoid cystic carcinoma, 143, 144
Adenomatoid odontogenic tumours, 47, 48
AIDS, 73, 159–160
Kaposi’s sarcoma, 123
major aphthae, 75
tuberculosis, 149
see also HIV infection
Albright syndrome, 65
Amalgam tattoo, 131, 132
Ameloblast-like cells, 39, 40
Ameloblastic fibroma, 49, 60
Ameloblastoma, 39–44
acanthomatous, 9, 42
basal cell, 39
cystic, 39, 44
desmoplastic, 41
follicular, 39, 40
granular cell, 39, 44
maxillary, 43, 44
plexiform, 39, 42
soft tissue 43, 44
stromal cysts, 39, 40
unicystic, 41
Ainelogenesis imperfecta, 1, 2
Amyloid deposits, 61, 62
Angina bullosa haemorrhagica, 87
Antinuctear factors, 89, 157
Aphthae
mafor, 75
181
recurrent, 75–76
see also ulcers
Apical granuloma, 11, 12
lipoma, 121
liposatcoma, 121
lymphangioma, 121, 122
Apical periodontitis, 11, 12
Areca nut chewing, 157
B
Basement membrane rone, 85, 88, 111 Bone
aneurysmal/solitaiy cyst, 37, 38
trabeculae of woven, 65, 66
see also Paget’s disease of bone
Bonelia (Treponemal vmcentii, 15, 16
Bullous erythema multiforme, 81–82
C
Calcification
adenomatoid odontogenic turnouts, 47 cemento-ossifying fibroma, 53, 66
CEOl, 45, 46
odontogenic cyst, 35, 36, 45, 46
odontoma, 51, 52
pleomorphic adenoma, 138
Calcifying epithelial odontogenic tumour (CEOT), 45, 46

Calculi, salivary, 147, 148
Candida endocrinopathy syndrome, 103
Candidosis
acute, 101, 102
chronic hyperplastic, 103, 104
chronic mucocutaneous syndromes, 103, 104 dentuie induced erythematous, 103 hairy leukoplakia,
159
HIV infection, 103, 159
Capillary haemangioma, 119, 120
Carcinoma in pleomorphic adenoma, 137, 143, 144
Carcinoma-in-situ, 105, 106
Cavernous haemangioma, 119, 120
Camental dysplasia, 53, 54
Cemento-osseous dysplasia, 55, 56
Cemento-ossifying fibroma, 53, 54, 56
Cementoblastoma, 13, 53, 54
Cementoma, 53, 54
Cheek, fibrous polyp, 113, 114
Cheek-biting, 95–96
Cheiubism, 67, 68
Cholesterol, radicular cyst clefts, 27, 28
Chondroma, 57
Clefts, radicular cysts, 27, 28
Connective tissue tumours, benign, 117–122
haemangioma, 119 120
neurilemmoma, 117, 118

neurofibroma, 117, 118
plexiform neurofibroma, 119, 120
traumatic neutoma, 117, 118

vascular leiomyoma, 121, 122
Crohn’s disease, 153, 154
Cystic ameloblastoma, 25, 26
D
Dental caries, 3–6
dentinal inactions, 5, 6
dentine, 4, 5, 6
precavitation stage, 3, 4
secondary enamel 3, 4
Dentigerous cysts, 30–31
eruption, 29, 30
Dentinal reactions, 5, 6
Dentine
budge, 9, 10
dead tracts, 5, 6
reacbonaiy, 5, 6
resorption, 13, 14
translucent zones, 5, 6
Dentine canes, 4, 5, 6
Dentinogenesis imperfecta, 1, 2
Denture granuloma, 113
Developmental defects, 1–2
Discoid lupus erythematosus, 89
Dyskeratosis, 105
Dysplasia, 91, 105–106
malignant change, 105
squamous cell carcinoma, 109
E
Ehlers–Danlos syndrome, 9
Enamel canes, secondary, 3, 4
Endarteritis
oblitorative, 71, 72
syphilitic leukoplakia, 99, 100
Eosinophilic granuloma, 63, 64
Epimyoepithelial islands, 147, 148 Epithelial atrophy, 91, 92
Epithelial attachment, chronic penodontitis,
19, 20
Epstein–Bair virus capsid antigen, 159, 160 Epulis
fibrous, 113, 114
giant cell, 115, 116

granular cell of newborn, 133
pregnancy, 115, 116
Erythema migrans, 97–98

Eiythema multiforme, bullous, 81–82
Erythroplakia, 107
Erythroplasia, 107, 108
F
Fibrosarcoma, 125, 126
Fihrnus dysplasia
cheruhism differential diagnosis, 67

monostotic, 65, 66
polyostotic, 65
Fibmus nodules, 113, 114
Fungal infection, 149, 150
Fusobacterium nucleatum, 16
G
Ghost cell, 35, 36
cyst, 45, 46
Giant cell epulis, 115, 116
Giant cell granuloma, cential of jaw, 61, 62
Giant cells
cremento-osseous dysplasia, 55, 56

cherubism, 67, 68
dentine resorption, 13, 14
fibrous dysplasia, 65, 66
histoplasmosis, 150
periodontal abscess, 22
sarcoidosis, 151, 152
tuberculosis, 149, 150
Wegener’s granulomatosis, 155
Gingiva, 15, 16
fibrous hyperplasia, 23, 24
sarcoidosis, 151
Gingival fibres, 15, 16
Gingival fibromatosis, 23, 24
Gingival necrosis, 15, 16
Gingival recession, 23, 24
Gingival swelling, 23, 24
Gingivitis
acute ulcerative, 15, 16
chronic, 17, 18
HIV infection, 159
Goblet cells, 27, 30
Granular cell epulis of newborn, 133
Granular cell tumour, 133, 134
Granuloma
denture, 113
histoplasmosis, 150
Melkersson Rosenthal syndrome, 153
midline lethal, 155
pyogenic, 113, 115, 116
sarcoidosis, 151, 152
tuberculous, 149, 150
Granulomatous disease, 149–156 182 actinomycosis, 151, 152
fungal infection, 149, 150
Melkersson Rosenthal syndrome, 153 midine granuloma syndrome, 155–156 nasopharyngeal T-cell
lymphoma, 155, 156
oral submucous fibrosis, 157, 168 orofacial gianulomatosis, 153, 154 sarcoidosis, 151, 152,

153
tuberculosis, 149, 150
H
Haemangioma, 119, 120
Hairy leukoplakia, 159, 160
Hand–Schüller–Christian disease, 63 Heerfordt syndrome, 153
Herpes
HIV infection, 159

labialis, 73
Herpes zoster of trigeminal area, 73
Herpetic stomatitis 73, 74
Histiocytes, 63, 64
Histiocytosis X, 63
Histoplasmosis, 149, 150
HIV infection, 159–160
aphthae, 76
candidosis, 103, 159
Kaposi’s sarcoma, 123, 159
tuberculosis, 149
see also AIDS
Hodgkin’s disease, 127
Human herpes virus 8 (HHV8), 123
Human papillomavirus, 107, 159
Hyaline bodies, 27, 28
Hypercementosis, 13, 14
Paget’s disease of bone, 69 70
Hyperchromatism, 105, 106
Hyperkeratosis, 91, 92
Hyperpaiathyiordism, 67, 68
giant cell epulis, 115
Hyperplasia, verrucous, 111
Hyperplastic lesions, 113–117
fibious nodules, 113, 114
pyogenic granuloma, 113, 116
Hypoparathyroidism, 103
I
Immunoglobulin G, 61, 83, 84
Immunosuppression, 101, 124
Incisive canal cyst, 33, 34
J
Jaw cysts, 25–38
bone cysts, 37–38
cystic odontogenic tumours, 35, 36
183
dentigerous, 30–31
nasolabial cyst, 33, 34
nasopalatine duct cyst, 33, 34 odontogenic keratocyst, 31–32 radicular, 25–28
without epithelial lining, 38–39
K
Kaposi’s sarcoma, 123–124
HIV infection, 123, 159
Keratinizing carcinoma early, 107, 108 Keratocyst
daughter cysts, 31, 34
odontogenic, 31–32
orthokeratinization, 31, 32
parakeratinization, 31, 32
Keratoses, 91–108
candidosis, 101, 102, 103, 104
cheek-biting, 95–96
dysplasia, 91, 105–106
erythema migrans, 97–98
erythroplasia, 107, 108
frictional, 99, 100
leukoedema, 95, 96
smoker’s, 99, 100
squamous cell papilloma, 107, 108 syphilitic leukoplakia, 99, 100 types, 91
white sponge naevus, 93–94
Koilocyte-like cells, 95–96

Koilocytes, 159, 160
HIV infection, 159
nasopharyngeal T-cell, 155, 156
L
Langerhans cell histiocytosis, 63, 64 Langhan’s giant cells, 149, 150
Leiomyoma, vascular, 121, 122
Letterer–Siwe disease, 63
Leukaemia, acute myelomonocytic, 23, 24 Leukoedema, 95, 96
Leukoplakia, 91
candidal, 103, 104
hairy, 159, 160

syphilitic, 99, 100
Lichen planus, 77–78, 79, 80
Lichenoid reactions, 79–80
Lip
adenoma, 140
cancer, 109, 111
herpes labialis, 73
Lipoma, 121
Liposarcoma, 121
Lupus erythematosus, 89–90
Lymphangioma, 121, 122
Lymphocytic infiltrate, perivascular, 157, 158
Lymphoma, 127–128
M
Malignant melanoma, 129, 132
Melanocytes, 129, 130
Melanocytic naevus, 129, 130
Melanotic neuroectodermal tumour, 47, 48 Melkersson Rosenthal syndrome, 153 Metabolic disturbance,
1
Metastases, 63
acinic cell carcinoma, 141
adenoid cystic carcinoma, 143, 144 carcinoma in pleomorphic adenoma, 143
osteosarcoma, 59, 60
squamous cell carcinoma, 109, 112
verrucous carcinoma, 111
Midline granuloma syndrome, 155–156 Monomorphic adenoma, 139, 140
Mucoceles, extravasation, 145, 146
Mucoepidermoid carcinoma, 141, 142 Mucosal tags, 153, 154
Mucous membrane pemphigoid, 85, 86, 88 Multiple endocrine neoplasia, 119
Multiple myeloma, 61, 62
Mycosis, HIV infection, 159
Myxoma, odontogenic, 51, 52
N
Naevi, pigmented, 129, 130
Naevus, white sponge, 93–94
Nasolabial cyst, 33, 34
Nasopalatine duct cyst, 33, 34
Nasopharyngeal T-cell lymphoma, 155, 156 Necrotizing ulcerative gingivitis, HIV infection,
159
Neurilemmioma, 117, 118
Neurofibroma, 117, 118
plexiform, 119
Neurofibromatosis, 117, 119
Neuroma, traumatic, 117, 118
Nikolsky’s sign, 83
Non-Hodgkin’s lymphoma, 127
Non-neoplastic bone disease, 65–73
cherubism, 67, 68
hyperparathyroidism, 67, 68
osteomyelitis, 71, 72
Paget’s disease of bone, 69–70
radiation injury, 71, 72
Nonodontogenic tumours of bone
central giant cell granuloma of jaw, 61, 62 chondroma, 57
Langerhans cell histiocytosis, 63, 64
multiple myeloma, 61, 62
osteochondroma, 57, 58
osteoma, 57, 58
osteosarcoma, 59–60 secondary, 63
O
Odontogenic carcinoma, clear cell, 45 Odontogenic cyst, calcifying, 25, 45, 46 Odontogenic
tumours, 39–57
adenomatoid, 47, 48
ameloblastic fibroma, 49, 50
ameloblastoma, 39–44
calcifying epithelial, 46, 47
calcifying odontogenic cyst, 45, 46
cemento-osseous dysplasia, 55, 56 cemento-ossifying fibroma, 53, 54, 56 cementoma/cemental

dysplasia, 53, 54
cystic, 35, 36
melanotic neuroectodermal tumour, 47, 48 myxoma, 51, 52
odontoma, 49, 51, 52
squamous, 49, 50
Odontoma, 51, 52
complex, 51, 52
compound, 49, 51, 52
Oral submucous fibrosis, 157, 158
Orofacial granulomatosis, 153, 154
Orthokeratosis, 91, 92
Osteoblasts, Paget’s disease of bone, 69, 70 Osteochondroma, 57, 58
Osteoclastic resportion, 21, 22
Osteoclasts
giant cell epulis, 115

hyperparathyroidism, 67, 68
Paget’s disease of bone, 69, 70
Osteoid, tumour, 59, 60
Osteoma, 57, 58
cartilage-capped, 57
Osteomyelitis, 71, 72
Osteoradionecrosis, 71, 72
Osteosarcoma, 59–60
gingival necrosis, 15, 16
Periodontal pockets, 19, 20
Periodontal tissue, normal, 15, 16
Periodontitis
apical, 11–12
bone loss, 21, 22
chronic, 19–20
advanced, 21, 22
HIV infection, 159
periapical, 11, 12
Phaemochromocytoma, 119
Pigmented lesions, 129–132
malignant melanoma, 129, 132
naevi, 129, 130
Pindborg tumour, 45
Plague 3, 4, 19, 20
candidosis, 101, 102, 103, 104
chronic gingivitis, 17
gingival swelling, 23, 24
parakeratotic, 104
thrush, 101, 102
Plasma cells antibody production, 17, 18
Pleomorphic adenoma, 135–138
carcinoma in 137, 143, 144
malignant change, 137, 143, 144 recurrence, 137
Pockets
intrabony, 21, 22
periodontal, 19, 20
Polyps, fibrous, 113, 114
Pregnancy epulis, 23, 24, 115, 116
Prickle cells
candidosis, 101
dysplasia, 105, 106
hairy leukoplakia, 160
leukoedema, 95, 96
Progonoma, 47
Pseudo-epitheliomatous hyperplasia, 133, 134
Pseudocysts, non-odontogenic, 37, 38
Pseudomembranous candidosis, 101
Psoriasis, 97
Pulp
abscess, 7, 8
calcification, 9, 10
cellulitis, 7, 8
hyperaemia, 7, 8
necrosis, 7
polyp, 9, 10
stones, 9, 10
Pulpitis, 7–10
closed, 7, 8
P
Paget’s disease of bone, 13, 14, 59, 69–70
Parakeratosis, 91, 92
Parathyroid tumour, 67
Pemphigoid
localized oral purpura differential diagnosis, 87 mucous membrane, 85, 86

Pemphigus vulgaris, 83–84
Periapical periodontitis, 11, 12
Periodontal abscess, 21, 22
Periodontal cyst, 11
Periodontal disease, 15–24 184 chronic gingivitis, 17, 18
chronic periodontitis, 19–20, 21, 22
185
open, 9–10
Purpura, localized oral, 87–88
Pyogenic granuloma, 113, 115, 116 Stomatitis, non-infective, 75–91
bullous erythema multiforme, 81–82
R
Radiation injury, 71, 72
Radicular cysts, 25, 28
clefts, 27, 28
epithelial lining, 25, 26
goblet cells, 27, 30
hyaline bodies, 27, 28
lateral, 25
residual, 25
Reed–Sternberg cells, 127
Resorption, 13, 14
Rests of Malassez
destruction, 11
proliferation, 25
Rhabdomyoma, 125, 126
Rhabdomyosarcoma, 125, 126
Rheumatoid factor, 89
Rickets 1, 2
Rushton bodies see hyaline bodies
S
Salivary calculi, 147, 148
Salivary gland cysts, 145–148
mucous retention, 145, 146
Salivary gland lesions in HIV infection, 159 Salivary gland tumours, 135–144
acinic cell carcinoma, 141, 142
adenocarcinoma, 143, 144
adenoid cystic carcinoma, 143, 144
carcinoma in pleomorphic adenoma, 137, 143, 144

monomrorphic adenoma, 139, 140 mucoepidermoid carcinoma, 141, 142
pleomorphic adenoma, 135–138 Warthin’s tumour, 139, 140
Sarcoidosis, 151, 152, 153
Sarcomas, 123–126
fibrosarcoma, 125, 126
Kaposi’s, 123–124
rhabdomyoma, 125, 126
rhabdomyosarcoma, 125, 126
Scleroderma, 157, 158
Secondary tumours see noital
Sialadenitis
chronic non-specific, 146, 148
duct dilatation, 147
Sicca syndrome, 147
Sjögren syndrome, 147, 148
Squamous cell carcinoma, 109–112 spread, 109, 111, 112
verrucous, 111, 112
Squamous cell papilloma, 107, 108
Stevens–Johnson syndrome, 81–82 Stomatitis, infective, 73–74
lichen planus, 77–78, 79, 80

lichenoid reactions, 79–80
lupus erythematosus, 89–99
mucous membrane pemphigoid, 85, 86, 88 oral purpura, 87–88
pemphigus vulgaris, 83–84
Streptococcus mutans, 3
Syphilitic leukoplakia, 99, 100
Systemic lupus erythematosus, 89
Systemic sclerosis, progressive, 157, 158
T
T lymphocytes, 77
Tetracycline pigmentation, 1, 2
Thrush, 101, 102
Thyroid medullary carcinoma, 119
Tongue
geographical, 97
histoplasmosis, 150
plexiform neurofibroma, 119
rhabdomyoma, 125, 126
systemic sclerosis, 157
tuberculous ulcer, 149
Trigeminal zoster, 73
Tuberculosis, 149, 150 Tumour osteoid, 59, 60 Tzanck cells, 84
U
Ulceration
HIV infection, 159
non-specific, 75, 76
Ulcers
Crohn’s disease, 153
tuberculous, 149, 150 see also aphthae
V
Varicella zoster, 73, 159
Vascular leiomyoma, 121, 122 Verrucous carcinoma, 111, 112 Verrucous hyperplasia, 111
Von Recklinghausen’s disease see
neurofibromatosis
W
Warthin’s tumour, 139, 140
Warts, oral viral, 107
Wegener’s granulomatosis, 155, 156 White sponge naevus, 93–94
186
DENTISTRY
Oral
Pathology
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Oral

Vimal K. Sikri COLOUR GUIDES

A Division of Arpit SikriScientific International

Other Related Titles in Medical and Dental Sciences

Dr. Arpit Sikri

Copyright © Scientific International

Published by:Vinod Kumar Jain, Scientific International (Pvt.) Ltd.

Amelogenesis imperfecta—hypoplastic or hypocalcified types

Microscopy Amelogenesis imperfecta

with regular tubules; remainder—a few irregular tubules, inclusion of small

Severe metabolic disturbances: typically affect enamel matrix producing linear

Tetracycline pigmentation: teeth usually of normal form but stained yellow,

Aetiology Bacteria: probably mainly acidogenic and glucan- forming strains of

Plaque: adherent meshwork of bacteria in polysaccharides, thickest in

Susceptible tooth surface and (possibly) immune responses.

Microscopy Pre-cavitation stage: bacterial acid leads to production of increasing

Degrees of demineralization in different zones are assessed by polarized light

Microscopy Dentine is demineralized by bacterial acids from bacteria spreading

Walls of tubules in softened dentine become distended by bacteria. Intervening

Traumatic exposure (cavity preparation, fracture or cracked tooth)

All degrees of severity may be encountered, namely: acute hyperaemia and

Predominantly mononuclear inflammatory cells (lymphocytes, plasma cells and

Other pulp changes

Microscopy Acute: accumulation of acute inflammatory cells (neutrophils) and

Chronic: low grade inflammation. Granulation tissue (fibroblasts and capillary

Epithelial content: rests of Malassez are often destroyed by inflammation. If not,

secondary (local inflammation, pressure from malposed tooth or tumour,

Idiopathic: progressive resorption by giant cells, mainly of dentine. There is

Usually lamellar—sequential deposition of layers of cementum forming smooth

Normal periodontal tissues

oral epithelium—extends from mucogingival junction to crest of gingival

Acute ulcerative gingivitis

poor oral hygiene

A smear shows this fusospirochaetal complex

Gingival necrosis and non-specific ulceration covered by slough containing

Aetiology Inflammatory response to bacterial plaque accumulating at the

Microscopy Plaque on tooth surface with inflammation sharply localized to

Persistence of bacterial plaque. Progression of inflammation with tissue

Many potent pathogens (e.g. Porphyromonas species, capnocytophaga,

1. Plaque and often calculus on tooth surface extending into pockets

2. Predominantly lymphoplasmacytic infiltrate in gingival margin and pocket

3. Rootward migration of epithelial attachment (Fig. 40).

Periodontal (lateral) abscess

Usually a complication of advanced periodontitis. It may be due to injury to the

Rapid acceleration of periodontal destruction. Destruction of epithelial pocket

increasing width and depth of pocket to form deep intrabony pocket.

Gradual destruction of gingival tissue, periodontal ligament and bone, all at

Drug-associated hyperplasia: produces bulbous swellings of interdental papillae.

Both show hyperplasia of gingival collagen with ‘stretching’ of elongated rete

Pulp death, apical periodontitis, proliferation of epithelial rests of Malassez,

The epithelial lining is stratified squamous in type and very variable in

Aspiration of cyst fluid typically also shows cholesterol as flat, rhomboid,

Competent enucleation of radicular cysts is curative. Complications of such

Cystic change in remains of enamel organ after completion of enamel formation.

15–18% of jaw cysts. The male : female ratio is more than 2 : 1.

Competent enucleation of dentigerous cysts with extraction of the contained

Eruption cysts usually rupture spontaneously.

Unknown. Probably originates from primordial odontogenic epithelium (any part

About 75% in body or ramus of mandible. Typically, expansive growth into

Oral Pathology Vimal K Sikri Colour Guides, MCQ's Arpit Sikri

Oral Pathology Vimal K Sikri Colour Guides, MCQ's Arpit Sikri

Oral Pathology Vimal K Sikri Colour Guides, MCQ's Arpit Sikri